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AIM: To investigate the effects of exercise preconditioning （EP） combined with electroacupuncture（ EA） on learning and memory ability of rats with vascular dementia（ VD）, and to explore role of hippocampal ferroptosis in this process. METHODS: Seventy-two male SD rats were randomly divided into non-EP group and EP group, with 36 rats in each group. The rats were subjected to EP, and subsequently to establish the VD model. The rats from non-EP group were randomly divided into sham group, model group （VD group） and VD-EA group, each with 12 rats, while those in EP group were randomly divided into EP-sham group, EP-VD group and EP-VD-EA group, each with 12 rats. All rats in EP group underwent 4 weeks of swimming exercise training, 5 d per week, 30 min per day. At the end of the 4th week, the rats in VD, EP-VD, EP-VD-EA and VD-EA groups were used to induce the VD model, and the rats in sham and EP-sham groups received a sham surgery to simulate the VD model. On the 7th day after successful modeling, the rats in EP-VD-EA and VD-EA groups were treated with EA for 4 weeks, 6 d per week, 30 min per day. At the end of the intervention, the learning and memory ability of the rats was evaluated using Morris water maze. Neuron morphology in the CA1 area of rat hippocampus was observed through Nissl staining. Ferrous ion （Fe2+）, malondialdehyde （MDA） and reduced glutathione（ GSH） contents in the rat hippocampal tissues were quantified using the colorimetric assay. The expression levels of ferroptosis-related proteins, nuclear factor E2-related factor 2（ Nrf2） and glutathione peroxidase 4（ GPX4）, in the hippocampal tissues were quantified by Western blot method. RESULTS: Compared with sham group, the rats in VD group exhibited longer mean evasion latency and decreased number of traversals across the plateau （P<0. 01）. The neurons in the CA1 region of the hippocampus were loose and disorganized, exhibiting an irregular cellular morphology. The hippocampal Fe2+ and MDA content was elevated, and the GSH content was reduced （P<0. 01）. The protein levels of hippocampal Nrf2 and GPX4 were decreased （P<0. 01）. Compared with VD group, the rats in EP-VD, EP-VD-EA and VD-EA groups showed a shorter average escape latency and an increased number of traversals across the plateau （P< 0. 05）. Neurons in the hippocampal CA1 area were more neatly arranged, showing regular cellular morphology. The hippocampal Fe2+ and MDA contents of the rats in EP-VD group were significantly reduced（P<0. 01）, while the GSH content was elevated （P<0. 05）. Hippocampal Fe2+ and MDA contents were significantly reduced and GSH contents were significantly increased in EP-EA and EA groups （P<0. 01）. The protein levels of hippocampal Nrf2 and GPX4 in EP-VD, EPVD-EA and VD-EA groups were significantly increased （P<0. 01）. CONCLUSION: Exercise preconditioning combined with EA improves learning and memory ability in VD rats by reducing hippocampal intra-neuronal iron overload, maintaining organismal redox homeostasis, and inhibiting ferroptosis. [ABSTRACT FROM AUTHOR]

BACKGROUND: β-amyloid protein and Tau protein have adverse effects on the cognitive function of Alzheimer’s disease patients, and Notch1 and Caspase-3 can regulate the expression of β-amyloid protein and Tau protein. It is not clear whether Notch1 and Caspase-3 mediate the process of aerobic exercise to improve the cognitive ability of Alzheimer’s disease patients. At present, there is a lack of studies on the effect of long-term aerobic exercise on the expression of Notch1 and Caspase-3 in the hippocampus of Alzheimer’s disease mice. OBJECTIVE: To observe the expression of Notch1 and Caspase-3 in the hippocampus of Alzheimer’s disease mice undergoing long-term aerobic exercise and to investigate the effects of Notch1 and Caspase-3 in Alzheimer’s disease mice. METHODS: Wild type and APP/PS1 double-transgenic Alzheimer’s disease mice aged 3 months were randomly divided into four groups: wild control group, wild exercise group, Alzheimer’s disease control group and Alzheimer’s disease exercise group, with 20 mice in each group. Mice in the control groups were not subjected to exercise, while those in the exercise groups received aerobic exercise intervention for 5 months. After the exercise intervention, Morris water maze was used to detect the spatial learning and memory ability of mice. Real-time PCR, immunofluorescence and western blot were used to detect the expressions of Aβ1-42, Tau, Notch1 and Caspase-3 in the hippocampal tissues of mice in each group. RESULTS AND CONCLUSION: The spatial learning and memory ability of Alzheimer’s mice was significantly worse than that of wild-type mice (P < 0.05). The spatial learning and memory ability of mice in the exercise groups were significantly better than that in the corresponding control groups (P < 0.05). The expressions of Aβ1-42, Tau, Notch1 and Caspase-3 in the hippocampus were significantly higher in the Alzheimer’s disease control group than the wild control group (P < 0.05) and were significantly lower in the Alzheimer’s disease exercise group than the Alzheimer’s disease control group (P < 0.05). To conclude, longterm aerobic exercise can improve the spatial learning and memory ability of Alzheimer’s disease mice, which may be related to the decreased expression of Notch1, Caspase-3, Aβ1-42 and Tau protein in the hippocampus of Alzheimer’s disease mice. [ABSTRACT FROM AUTHOR]

Copyright of Modern Food Science & Technology is the property of Editorial Office of Modern Food Science & Technology and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Chinese Journal of Preventive Veterinary Medicine / Zhongguo Yufang Shouyi Xuebao is the property of Chinese Journal of Preventive Veterinary Medicine Editorial Office and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Objective To investigate the mechanism of IGF2/JAK2/STAT3 on learning and memory impairment induced by aluminum maltol in rats. Methods A total of 32 SD rats were divided into normal saline control group and low, medium and high maltol aluminum exposure groups (10, 20 and 40 µmol/kg) by random number table, respectively, and intraperitoneally injected every other day for three months. After exposure, Morris water maze was applied to examine the learning and memory ability of rats, and HE staining was used to check the arrangement of hippocampal neurons. Real-time fluorescence quantitative PCR was applied to detect the relative expression level of IGF2 mRNA in hippocampus of rats. Western Blotting was used for detecting the relative protein expression levels of Cleaved Caspase3, IGF2, p-JAK2 (Tyrl007/1008), and p-STAT3 (Ser727) in the hippocampus of rats. Results With the increase of aluminum dose, the escape latency of rats in the same day was prolonged, and the residence time in the target quadrant and the times of crossing the platform were gradually reduced (F = 7. 900, P = 0.001; F = 6.693, P = 0.002) . HE staining results showed that the number of neurons in CA1 region of hippocampus gradually decreased and the arrangement of neurons was obviously loose with the increase of aluminum dose (F = 25. 947, P < 0.001) . With increasing aluminum dose, apoptosis-associated protein Bel-2 levels decreased gradually (F = 83. 235, P < 0.001), Bax (F = 153. 189, P < 0.001) and Cleaved Caspase3 (F = 11.636, P < 0.01) levels was gradually increased, and the relative expression levels of IGF2 mRNA and IGF2, p-JAK2 (Tyr1007/1008), p-STAT3 (Ser727) proteins decreased gradually with the increase of aluminum dose (F = 18. 423, P < 0.001; F = 11.072, P = 0.001; F = 55. 161, P < 0.001; F = 10.481, P = 0.001). Conclusion Aluminum maltol can induce cell apoptosis by inhibiting IGF2/JAK2/STAT3 pathway, which could damage the learning and memory ability of rats. [ABSTRACT FROM AUTHOR]

BACKGROUND: Exercise improves Alzheimer’s disease, dementia, and age-related cognitive abilities. A potential mediator between exercise and these health benefits may be adult hippocampal neurogenesis. Therefore, it is of great significance to explore whether and how exercise affects the adult hippocampal neurogenesis process in Alzheimer’s disease mice. OBJECTIVE: To observe the effect of aerobic exercise on adult hippocampal neurogenesis of Alzheimer’s disease mice, and to explore whether aerobic exercise can promote their adult hippocampal neurogenesis. METHODS: Three-month-old wild-type (C57BL/6Jnju) and APP/PS1 double transgenic Alzheimer’s disease mice were randomly divided into four groups: wild control group, wild exercise group, Alzheimer’s disease control group and Alzheimer’s disease exercise group, with 20 mice in each group. The control group did not do exercise, and the exercise group did aerobic exercise for 5 months. After exercise intervention, real-time PCR, immunofluorescence and western blot assay were used to detect the expression levels of DCX, Ki67, βIII-tubulin and NeuN in the hippocampal tissue of mice in each group. RESULTS AND CONCLUSION: The expressions of DCX, βIII-tubulin and NeuN in the hippocampal dentate gyrus in the Alzheimer’s disease control group were significantly lower than those in the wild control group (P < 0.05). The expressions of DCX, Ki67, βIII-tubulin and NeuN were significantly higher in the hippocampal dentate gyrus in the Alzheimer’s disease exercise group than those in the Alzheimer’s disease control group (P < 0.05). It is indicated that longterm aerobic exercise intervention can strengthen the proliferation, migration and differentiation of neurons during adult hippocampal neurogenesis and significantly increase the number of neuronal precursor cells and new neurons in Alzheimer’s disease mice. [ABSTRACT FROM AUTHOR]

The abnormality in N6-methyladenosine (m6A) methylation is involved in the course of Alzheimer's disease (AD), while the intervention of 27-Hydroxycholesterol (27-OHC) can affect the m6A methylation modification in the brain cortex. Disordered gut microbiota is a key link in 27-OHC leading to cognitive impairment, and further studies have found that the abundance of Roseburia intestinalis in the gut is significantly reduced under the intervention of 27-OHC. This study aims to investigate the association of 27-OHC, Roseburia intestinalis in the gut, and brain m6A modification in the learning and memory ability injury. In this study, 9-month-old male C57BL/6J mice were treated with antibiotic cocktails for 6 weeks to sweep the intestinal flora, followed by 27-OHC or normal saline subcutaneous injection, and then Roseburia intestinalis or normal saline gavage were applied to the mouse. The 27-OHC level in the brain, the gut barrier function, the m6A modification in the brain, and the memory ability were measured. From the results, we observed that 27-OHC impairs the gut barrier function, causing a disturbance in the expression of m6A methylation-related enzymes and reducing the m6A methylation modification level in the brain cortex, and finally leads to learning and memory impairment. However, Roseburia intestinalis supplementation could reverse the negative effects mentioned above. This study suggests that 27-OHC-induced learning and memory impairment might be linked to brain m6A methylation modification disturbance, while Roseburia intestinalis, as a probiotic with great potential, could reverse the damage caused by 27-OHC. This research could help reveal the mechanism of 27-OHC-induced neural damage and provide important scientific evidence for the future use of Roseburia intestinalis in neuroprotection. [ABSTRACT FROM AUTHOR]

Active physical exercise can effectively alleviate the pathological process of chronic cerebral ischemia (CCH) and improve learning and memory ability. This paper reviews the possible biological mechanisms of aerobic exercise to delay the pathological process of chronic cerebral ischemia and improve learning and memory. Previous studies have found that aerobic exercise can improve the neuroprotective effect, enhance the plasticity of hippocampal synapses, improve the activity of the upper and lower pathways of hippocampal tissue, and improve learning and memory ability. However, the intervention effect of aerobic exercise on chronic cerebral ischemia should be fully considered at the intervention time, and the intervention effect is also different. [ABSTRACT FROM AUTHOR]

BackgroundFormaldehyde and benzene homologues are common environmental pollutants, and their neurotoxicity has aroused widespread concern.ObjectiveTo investigate the effect of taurine on cognitive impairment after exposure to formaldehyde and benzene analogues in young rats.MethodsTwenty four-week old SD rats were randomly divided into four groups, with six rats in each group: control group (clean air), model group (5 mg·m−3 formaldehyde + 5 mg·m−3 benzene + 10 mg·m−3 toluene + 10 mg·m−3 xylene), low-dose taurine intervention group (5 g·L−1 taurine + mixture of formaldehyde and benzene analogues), and high-dose taurine intervention group (10 g·L−1 taurine + formaldehyde and mixture of benzene analogues), and the exposure was administered by oral and nasal aerosol inhalation for 28 d. At the end of exposure, the learning and memory ability of rats in each group was measured by Morris water maze test. After the behavioral test, the rats were anesthetized and neutralized, and the brain tissue was harvested for histopathological and molecular biological tests. The apoptosis rate of neurons in hippocampal CA1 area was detected by Tunel assay, and the expression levels of apoptosis-related proteins such as caspase 3, bax, and bcl-2 in hippocampal tissue were detected by Western blotting.ResultsThe growth and development of rats in each group were good during inhalation. During the Morris water maze experiment, the escape latencies of rats in the taurine intervention groups were not different from that in the control group (P>0.05) from day 3 to day 5 of training, while the escape latency of rats in the model group was significantly higher than that in the control group (P 0.05), while the two variables in the model group and low-dose taurine intervention group were significantly lower than those in the control group (P 0.05). The expression levels of caspase 3 and bax in the model group were higher than those in the control group and low-dose or high-dose taurine intervention groups (P

This research adopted the D-galactose induced senility mice as the research object, under the condition of constant energy control, different protein content of feeding groups was designed. Mice were under dietary intervention for 8 weeks, by analyzing the Morris water maze data, brain tissue slice and liver tissue antioxidant capacity to explore the anti-aging effect of protein nutrition in Guangxi longevity dietary patterns. The results showed that: Compared with the high (P/C=1/2), medium (P/C=1/3) and low (P/C=1/5) protein diet groups, the escape latency of mice in P/C=1/4 (protein/carbohydrate) group significantly decreased (P P/C=1/5 group > P/C=1/3 group > young control group > P/C=1/2 group > aging control group. In summary, mice in P/C=1/4 low-protein diet group can effectively resist the senior-induced injury of D-galactose, and maintain strong learning and memory ability and antioxidant ability, thus showing strong anti-aging effect. The results of this study would provide a theoretical basis for the relationship between dietary protein nutrition and health as well as longevity.

IntroductionFluoride is considered an environmental pollutant that seriously affects organisms and ecosystems, and its harmfulness is a perpetual public health concern. The toxic effects of fluoride include organelle damage, oxidative stress, cell cycle destruction, inflammatory factor secretion, apoptosis induction, and synaptic nerve transmission destruction. To reveal the mechanism of fluorosis-induced brain damage, we analyzed the molecular mechanism and learning and memory function of the SIRT1-mediated BDNF–TrkB signaling pathway cascade reaction in fluorosis-induced brain damage through in vivo experiments.MethodsThis study constructed rat models of drinking water fluorosis using 50 mg/L, 100 mg/L, and 150 mg/L fluoride, and observed the occurrence of dental fluorosis in the rats. Subsequently, we measured the fluoride content in rat blood, urine, and bones, and measured the rat learning and memory abilities. Furthermore, oxidative stress products, inflammatory factor levels, and acetylcholinesterase (AchE) and choline acetyltransferase (ChAT) activity were detected. The pathological structural changes to the rat bones and brain tissue were observed. The SIRT1, BDNF, TrkB, and apoptotic protein levels were determined using western blotting.ResultsAll rats in the fluoride exposure groups exhibited dental fluorosis; decreased learning and memory abilities; and higher urinary fluoride, bone fluoride, blood fluoride, oxidative stress product, and inflammatory factor levels compared to the control group. The fluoride-exposed rat brain tissue had abnormal AchE and ChAT activity, sparsely arranged hippocampal neurons, blurred cell boundaries, significantly fewer astrocytes, and swollen cells. Furthermore, the nucleoli were absent from the fluoride-exposed rat brain tissue, which also contained folded neuron membranes, deformed mitochondria, absent cristae, vacuole formation, and pyknotic and hyperchromatic chromatin. The fluoride exposure groups had lower SIRT1, BDNF, and TrkB protein levels and higher apoptotic protein levels than the control group, which were closely related to the fluoride dose. The findings demonstrated that excessive fluoride caused brain damage and affected learning and memory abilities.DiscussionCurrently, there is no effective treatment method for the tissue damage caused by fluorosis. Therefore, the effective method for preventing and treating fluorosis damage is to control fluoride intake.

High levels of Aβ accumulation leads to hippocampal damage, resulting in impaired oxidative stress responses and synaptic function, and ultimately cognitive impairment. Here, we investigated the effects of olfactory stimuli on Aβ1-42-induced AD models using an essential oil containing drug-food congeners. Through behavioral experiments, we found that the learning and memory ability of rats was affected to a certain extent after the injection of Aβ1-42 into the lateral ventricle, and the olfactory stimulation could improve the cognitive impairment caused by Aβ1-42. In addition, we applied network pharmacology to predict multiple possible anti-AD mechanisms based on the composition of essential oils used as olfactory stimuli. We selected the effects of olfactory stimuli on oxidative stress response and synaptic function, and found that Nrf2 signaling pathway and NMDAR/PSD95/nNOS signaling pathway were activated. Our results suggest that olfactory stimulation holds promise as a treatment for cognitive impairment.

Copyright of Modern Food Science & Technology is the property of Editorial Office of Modern Food Science & Technology and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Chinese Journal of Contemporary Pediatrics is the property of Xiangya Medical Periodical Press and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Our previous studies have shown that the nutritional properties of peanut meal after fermentation are markedly improved. In this study, in order to facilitate the further utilisation of peanut meal, we investigated the effects of its fermentation extract by Bacillus natto (FE) on cognitive ability, antioxidant activity of brain and protein expression of hippocampus of ageing rats induced by d-galactose. Seventy-two female sd rats aged 4–5 months were randomly divided into six groups: normal control group, ageing model group, FE low-dose group, FE medium-dose group, FE high-dose group and vitamin E positive control group. Morris water maze (MWM) test was performed to evaluate their effects on learning and memory ability in ageing rats. Superoxide dismutase (SOD) activity and malondialdehyde (MDA) content of brain, HE staining and the expression of γ-aminobutyric acid receptor 1 (GABABR1) and N-methyl-d-aspartic acid 2B receptor in the hippocampus of rats were measured. The results show that FE supplementation can effectively alleviate the decrease of thymus index induced by ageing, decrease the escape latency of MWM by 66·06 %, brain MDA by 28·04 %, hippocampus GABABR1 expression by 7·98 % and increase brain SOD by 63·54 % in ageing model rats. This study provides evidence for its anti-ageing effects and is a research basis for potential nutritional benefits of underutilised food by-products. [ABSTRACT FROM AUTHOR]

Background and Objectives: Zeaxanthin (ZEA) as one of the biologically active phytochemicals presents a neuroprotective effect. Since ZEA may play its anti-oxidative role in neurodegenerative diseases including Alzheimer's disease (AD), we hypothesized cognitive defects could be prevented or deferred by ZEA pre-treatment. Methods and Study Design: All the rats were randomly divided into four groups (control, Aβ1–42, ZEA, and ZEA + Aβ groups). Learning and memory ability of rats, cerebrovascular ultrastructure changes, the redox state, endothelin-1 (ET-1) level, and amyloid-β peptide (Aβ) level in plasma and the Aβ transport receptors which are advanced glycation end products (RAGEs) and LDL receptor-related protein-1 (LRP-1) and interleukin-1β (IL-1β) expressions in the cerebrovascular tissue were measured in the present study. Results: The escape latency and frequency of spanning the position of platform showed significant differences between the Aβ group and ZEA treatment groups. ZEA could prevent the ultrastructure changes of cerebrovascular tissue. In addition, ZEA also showed the protective effects on regulating redox state, restraining ET-1 levels, and maintaining Aβ homeostasis in plasma and cerebrovascular. Moreover, the disordered expressions of RAGE and LRP-1 and IL-1β induced by Aβ1–42 could be prevented by the pre-treatment of ZEA. Conclusion: ZEA pre-treatment could prevent learning and memory impairment of rats induced by Aβ1–42. This neuroprotective effect might be attributable to the anti-oxidative and anti-inflammatory effects of ZEA on maintaining the redox state and reducing the Aβ level through regulating the Aβ transport receptors and inflammatory cytokine of the cerebrovascular tissue. [ABSTRACT FROM AUTHOR]

In this study, we aimed to observe the effects of Loofah cylindrica (LC) extract on learning and memory ability, brain tissue morphology, and immune function of aging mice. Kunming mice were selected and randomly divided into a control group, a positive control group, an aging group, and three dose groups. Three dose groups were administered 187.5, 375, and 750 mg/kg of LC extract, respectively. Except for the control group, the mice in any other group were continuously subcutaneously injected d-galactose on the back and neck. Platform tests and Morris water maze (MWM) were adopted to test the learning and memory ability of each group. The brain index, thymus index, and spleen index of each group were determined by the organ-to-body ratio method. The enzyme-linked immunosorbent assay was performed to measure the concentration of cytokines interleukin 2 and interferon gamma and the proliferation activity of T lymphocytes in mouse serum. In addition, the hematoxylin and eosin staining was employed to observe the morphological changes in mouse brain tissues of each group. The results show that the aging group made more errors in the platform test, had longer escape latency, shorter swimming time in the platform quadrant, and fewer platform crossings in the MWM; much fewer brain tissue cells; and smaller brain index, thymus index, and spleen index. The LC extracts (375 and 750 mg/kg) can significantly antagonize the changes in the above indices. It can be concluded that LC extract can improve the learning and memory of aging mice, enhance their immune activity, and delay the aging process.

Background and ObjectivesZeaxanthin (ZEA) as one of the biologically active phytochemicals presents a neuroprotective effect. Since ZEA may play its anti-oxidative role in neurodegenerative diseases including Alzheimer’s disease (AD), we hypothesized cognitive defects could be prevented or deferred by ZEA pre-treatment.Methods and Study DesignAll the rats were randomly divided into four groups (control, Aβ1–42, ZEA, and ZEA + Aβ groups). Learning and memory ability of rats, cerebrovascular ultrastructure changes, the redox state, endothelin-1 (ET-1) level, and amyloid-β peptide (Aβ) level in plasma and the Aβ transport receptors which are advanced glycation end products (RAGEs) and LDL receptor-related protein-1 (LRP-1) and interleukin-1β (IL-1β) expressions in the cerebrovascular tissue were measured in the present study.ResultsThe escape latency and frequency of spanning the position of platform showed significant differences between the Aβ group and ZEA treatment groups. ZEA could prevent the ultrastructure changes of cerebrovascular tissue. In addition, ZEA also showed the protective effects on regulating redox state, restraining ET-1 levels, and maintaining Aβ homeostasis in plasma and cerebrovascular. Moreover, the disordered expressions of RAGE and LRP-1 and IL-1β induced by Aβ1–42 could be prevented by the pre-treatment of ZEA.ConclusionZEA pre-treatment could prevent learning and memory impairment of rats induced by Aβ1–42. This neuroprotective effect might be attributable to the anti-oxidative and anti-inflammatory effects of ZEA on maintaining the redox state and reducing the Aβ level through regulating the Aβ transport receptors and inflammatory cytokine of the cerebrovascular tissue.

Dysregulation of cholesterol metabolism and its oxidative products—oxysterols—in the brain is known to be associated with neurodegenerative diseases. It is well-known that 27-hydroxycholesterol (27-OHC) and 24S-hydroxycholesterol (24S-OHC) are the main oxysterols contributing to the pathogenesis of Alzheimer's disease (AD). However, the molecular mechanism of how 27-OHC and 24S-OHC cause cognitive decline remains unclear. To verify whether 27-OHC and 24S-OHC affect learning and memory by regulating immune responses, C57BL/6J mice were subcutaneously injected with saline, 27-OHC, 24S-OHC, 27-OHC+24S-OHC for 21 days. The oxysterols level and expression level of related metabolic enzymes, as well as the immunomodulatory factors were measured. Our results indicated that 27-OHC-treated mice showed worse learning and memory ability and higher immune responses, but lower expression level of interleukin-10 (IL-10) and interferon (IFN-λ2) compared with saline-treated mice, while 24S-OHC mice performed better in the Morris water maze test than control mice. No obvious morphological lesion was observed in these 24S-OHC-treated mice. Moreover, the expression level of interleukin-17A (IL-17A), granulocyte-macrophage colony-stimulating factor (GM-CSF) and macrophage inflammatory protein 3α (MIP-3α) were significantly decreased after 24S-OHC treatment. Notably, compared with 27-OHC group, mice treated with 27-OHC+24S-OHC showed higher brain 24S-OHC level, accompanied by increased CYP46A1 expression level while decreased CYP7B1, retinoic acid-related orphan receptor gamma t (RORγt) and IL-17A expression level. In conclusion, our study indicated that 27-OHC is involved in regulating the expression of RORγt, disturbing Th17/Treg balance-related immune responses which may be associated with the learning and memory impairment in mice. In contrast, 24S-OHC is neuroprotective and attenuates the neurotoxicity of 27-OHC. [ABSTRACT FROM AUTHOR]

Objectives: To observe the effect of simulated repeated transcranial acupuncture (rTAS) on learning and memory abilities and cerebral microvascular flow in vascular dementia (VD) model rats, so as to explore the potential mechanism of rTAS in treating VD., Methods: Thirty-two Wistar rats were randomly divided into normal, model, acupuncture and rTAS groups ( n =8 rats in each group). The VD model was established by permanent ligation of bilateral common carotid arteries. For rats of the acupuncture group, "Baihui" (GV20) and "Shenting" (GV24) were needled, and for rats of the rTAS group, GV20 and GV24 were stimulated by simulated repeated transcranial manipulation (200 r/min, for 5 min). The treatment was conducted once daily for 14 days. After the intervention, learning and memory abilities were evaluated using the Morris water maze test. Laser speckle technology was used to measure the average cerebral microvascular flow. ELISA was performed to measure the contents of vascular endothelial growth factor (VEGF), endothelin-1 (ET-1), nitric oxide (NO), and inducible nitric oxide synthase (iNOS) in the hippocampal tissues., Results: In comparison with the normal group, the escape latency of rats in the model group was prolonged ( P <0.01), and the times of crossing the platform were decreased ( P <0.01). The average cerebral microvascular flow and the VEGF content in the hippocampus were significantly decreased, while the contents of NO, iNOS, and ET-1 were significantly increased ( P <0.01). In comparison with the model group, the escape latency was significantly shortened ( P <0.01), the average cerebral microvascular flow and VEGF content in the hippocampus were significantly increased ( P <0.05, P <0.01), while contents of iNOS were significantly decreased ( P <0.05, P <0.01) in both acupuncture and rTAS groups；and the times of crossing the platform were increased ( P <0.01), the contents of NO and ET-1 in hippocampus were significantly decreased ( P <0.01) in the rTAS group. The effects of rTAS were significantly superior to those of acupuncture in up-regulating the average cerebral microvascular flow ( P <0.05) and VEGF content ( P <0.01), and down-regulating the NO, iNOS and ET-1 contents ( P <0.01, P <0.05)., Conclusions: rTAS can increase cerebral microvascular flow, improve spatial cognition and enhance learning and memory abilities of VD rats. The underlying mechanism may be involved in promoting angiogenesis, improving endothelial function and mitigating oxidative stress.

Synaptic impairment results in cognitive dysfunction of Alzheimer’s disease (AD). As a plant extract, it is found that DL-3-n-butylphthalide (L-NBP) rescues abnormal cognitive behaviors in AD animals. However, the regulatory effects of L-NBP on synaptic plasticity remains unclear. APP/PS1 mice at 12 months old received oral L-NBP treatment for 12 weeks. A water maze test assessed cognitive performances. In vitro patch-clamp recordings and in vivo field potential recordings were performed to evaluate synaptic plasticity. The protein expression of AMPA receptor subunits (GluR1 and GluR2) and NMDA receptor subunits (NR1, NR2A, and NR2B) was examined by Western blot. In addition, glutaminase activity and glutamate level in the hippocampus were measured by colorimetry to evaluate presynaptic glutamate release. L-NBP treatment could significantly improve learning and memory ability, upregulate NR2A and NR2B protein expressions, increase glutaminase activity and glutamate level in the hippocampus, and attenuate synaptic impairment transmission in the AD mice. L-NPB plays a beneficial role in AD mice by regulating NMDA receptor subunits’ expression and regulating presynaptic glutamate release.

To investigate whether microcystin-LR (MC-LR) influences children’s cognitive function and memory ability, we measured serum MC-LR and whole blood lead levels in 697 primary students, and collected their academic and neurobehavioral test scores. The median of serum MC-LR levels was 0.80 µg/L (the value below the limit of detection to 1.67 µg/L). The shapes of the associations of serum MC-LR levels (cut-point: 0.95 µg/L) with scores on academic achievements, digit symbol substitution test and long-term memory test were parabolic curves. Logistic regression analysis showed that MC-LR at concentrations of 0.80–0.95 µg/L was associated with the increased probability of higher achievements on academic achievements [odds ratio (OR) = 2.20, 95% confidence interval (CI): 1.28–3.79], and also with scores on digit symbol substitution test (OR = 1.73, 95% CI: 1.05–2.86), overall memory quotient (OR = 2.27, 95% CI: 1.21–4.26), long-term memory (OR = 1.85, 95% CI: 1.01–3.38) and short-term memory (OR = 2.13, 95% CI: 1.14–3.98) after adjustment for confounding factors. Antagonism of MC-LR and lead on long-term memory was observed (synergism index = 0.15, 95% CI: 0.03–0.74). In conclusion, serum MC-LR at concentrations of 0.80–0.95 µg/L was positively associated with higher scores on cognitive and neurobehavioral tests, and antagonism between MC-LR at concentrations of 0.80–1.67 µg/L and lead exposure was obviously observed on long-term memory in children. Concerning that MC-LR is a neurotoxin at high doses, our observation is interesting and need further investigation.

The aim of this study was to investigate the anti-ageing effect of Yisui moxibustion on regulating the klotho protein and insulin (INS)/IGF-1 signalling cascade in d-galactose mice. Sixty male Kunming mice were randomly divided into five groups after the Morries test: the normal sodium, model, moxa cone moxibustion 1 and 2, and sham groups. The treatment and model were given d-galactose injection for 70 days, while mice in the normal sodium group were injected the same dosage of normal sodium. From day 13 after the first injection, the three treatment groups were treated every day for 58 days. The INS and klotho in the cerebral tissues were measured. p-Akt, p-FoxO3a, Klotho, SOD2 expression were observed immunohistochemically. The escape latency of mice in the model and sham were significantly prolonged, and the spanning original platform times were significantly decreased compared with the normal sodium and moxa cone moxibustion 1 and 2 (p

Objective:To explore the effects of electro-acupuncture at Changqiang acupoint on the BDNF protein expression in hippocampal CA3 region in rats with autism.Methods:Autism rat model was made by intraperitoneal injection of pregnant rats with valproate sodium (VPA).A total of 24 autism rats were divided into model group, Changqiang group and non-acupoint group, with 8 rats in each group;8 normal litter mate rat were used as blank group. The Changqiang group acupuncture Changqiang point 0.3 inch, using 0.5 inch homemade bipolar conjoined needle, electro-acupuncture 20 min,20 days a course of treatment; The non-acupoint group adopts the same method as the Changqiang group except the acupoints are different; The blank group and model group were kept under the same condition. Rats were weighed at different time points after birth (PN7,PN14,PN23 and PN34),using Morris water maze to evaluate learning and memory ability of rats, and using immunohistochemical to evaluate BDNF protein expression in hippocampal CA3 area of rats.Results:1. Weight: At PN34, weight of Changqiang group was higher than the model group (PP>0.05).2. Morris sater maze: Compared with the blank group, average latency time of the model group was significantly prolonged, quadrant swimming time/total time of the original platform decreased significantly, with statistically significant difference (PPP>0.05). 3. Immunohistochemistry: Compared with the blank group, the mean gray value of BDNF protein in model group increased significantly, with statistically significant differences (PPP>0.05).Conclusion:Electro-acupuncture at Changqiang acupoint can increase the expression of BDNF protein in the hippocampus CA3 region of autistic rats, and improving the growth, development and learning and memory abilities of autistic rats.

Objective: The aim of this study was to reveal the effect of butylphthalide on learning and memory ability of rats with ischemic stroke, and the regulation of butylphthalide on 5-HT1A receptor and PKA signaling pathway in hippocampus of rats. Male Sprague-Dawley (SD) rats were randomly divided into a sham group, a model group and a butylphthalide group (n=15). A model of middle cerebral artery occlusion was established in rats in the butylphthalide group, and the rats were administrated orally with butylphthalide at a dose of 60 mg / kg per day for 2 weeks. The sham group and the model group were administered orally with equal volume of corn oil for 2 weeks. After the treatment, neurological deficit assessment and Morris water maze test were performed on each group of rats (n=15). The infarcted area was detected by magnetic resonance imaging (MRI) (n=15). ELISA was performed to determine PKA kinase activity in hippocampus (n=6). Intracellular [Ca2+] concentration in the hippocampus was measured using a calcium detection kit (n=6). Western blot was used to detect the expression of serotonin (1A) receptor (5-HT1A), N-methyl-D-aspartate receptor 1 (NMDA1) and 琢-amino-3-hydroxy-5-methyl-4-isoxazole-propionic acid receptor (AMPA1) in hippocampus (n=6). Compared with the model group: the escape latency of rats in the butylphthalide group were significantly reduced, but the number of crossing platforms was greatly increased (P<0.05); the neurologic deficit score and cerebral infarction volume of rats were tremendously reduced (P<0.05); the PKA kinase activity and intracellular [Ca2+] concentration in rats increased dramatically (P<0.05); the relative expression of 5-HT1A protein decreased markedly in rats in the phthalein group, while the phosphorylation level of AMPA1 and NMDA1 increased sharply (P<0.05). Butylphthalide can improve the learning and memory ability of rats with ischemic stroke, and down-regulate the activity of 5-HT1A receptor, and activate the PKA signaling pathway in hippocampus. [ABSTRACT FROM AUTHOR]

To observe the effect of the early intervention with moxibustion at "Shènshū (肾俞 BL23) " on learning and memory of Alzheimer's disease (AD) rats modeled by ovariectomy and D-Galactose (D-Gal) injection and the effect on Ca2+/CaMKII/CREB signaling pathway so as to provide the evidence for the acupoint selection in the early intervention with acupuncture and moxibustion for AD. Sixty female SD rats at the age of 3 months were selected and randomly divided into a normal group, a sham-operation group, a model group, a "BL23" group, a "Wèishū" (胃俞BL21) group, and a non-acupoint group, 10 rats in each group. Except in the normal group and the sham-operation group, bilateral ovaries were removed in the other 4 groups. 3 days after the operation, D-Gal was injected intraperitoneally at a dose of 150 mg/kg/d for 90 days to establish AD rat model. In the sham-operation group, only the peripheral fat of ovarian was removed and 0.9% normal saline was injected intraperitoneally of the same dose for 90 days. In the "BL23" group, the "BL21" group and the non-acupoints group, since the 2nd day after ovariectomy, moxibustion was applied at 9:00 a.m. every day in the rats. The rats were fixed on a fixed table, the mild moxibustion with self-prepared moxa stick was applied to bilateral "BL23" "BL21" and the non-acupoint of each rat, the ignited end of moxa stick was 2 cm to 3 cm far from skin surface. The infrared thermometer was adopted to measure the temperature of the epidermis of each acupoint from time to time so as to maintain the local temperature to be (41 ± 0.5) °C. Mild moxibustion lasted for 10 min each time, consecutively for 5 days a week and at an interval of 2 days. The total consecutive intervention duration was 12 weeks. In the normal group and the sham-operation group, no moxibustion intervention was performed, but the rats were restricted in a same way during the experiment. At the end of modeling and intervention, water maze test was adopted to detect the learning and memory abilities of rats in each group. The western blotting was used to detect the expressions of p-CREB, p-CaMKII, CaMKII and CREB in hippocampus of rats in each group. (1)Navigation test: since Day 72, compared with the sham-operation group, the escape latencies in all of the consecutive 5 days were longer in the model group (all P < 0.05). Since Day 73, compared with the normal group, the escape latency in all of the consecutive 4 days was shorter in the "BL23" group (all P < 0.05). (2) Times across platform: compared with the normal group, the number of times consecutively crossing the platform was lower in the model group (P < 0.05). After moxibustion, compared with the model group, the number of times across platform was higher in the "BL23" group, indicating a statistical significance (P < 0.05). (3)Moving track of water maze spatial probe: the "tendency" strategy was displayed in the normal group and the sham operation group. The "marginal" strategy, which is commonly seen in the AD rats, was displayed in the model group. The "random" strategy was displayed in the "BL23" group. The "marginal" strategy was presented in the "BL21" group and the non-acupoint group. (4) Expressions of hippocampal P-CAMKII, CAMKII, CREB and P-CREB in the rats: compared with the normal group, the phosphorylation degrees of CAMKII and CREB were significantly reduced (both P < 0.05) in the model group. In 12 weeks of moxibustion, compared with the model group, the levels of P-CAMKII and P-CREB were increased in the "BL23" group and the "BL21" group (all P < 0.05) and the levels in the "BL23" group were higher than that of the "BL21" group and the non-acupoint group (all P < 0.05). Moxibustion at "BL23" achieves a better effect in improving the learning and memory of AD rats modeled by ovariectomy and D-Gal injection as compared with moxibustion at "BL21" and the non-acupoint. The effect mechanism is potentially related to the effective activation of Ca2+/CaMKII/CREB signaling pathway. [ABSTRACT FROM AUTHOR]

Studies from our group and others have reported that 30 mW/cm2 microwave could damage the structures of rat hippocampus, as well as impair the neuronal functions. The neuroprotective effects of astragaloside, purified from Astragalus membranaceus, have been demonstrated in animal models of neurodegenerative diseases. In this study, we found that 30 mW/cm2 microwave impaired spatial learning and memory ability in rats, while astragaloside could significantly alleviate the injuries. The pathological analysis also showed that astragaloside protected neurons from microwave-induced damages, such as mitochondrial swelling and cavitation, rough endoplasmic reticulum swelling and dilation, synaptic gap disappearing, and vesicle aggregation. Moreover, microwave-induced structural damage of synapse resulted in downregulation of acetylcholine, an important neurotransmitter for information transmission, while astragaloside could protect the structure of synapse, as well as restore the acetylcholine level in rat hippocampus. Furthermore, astragaloside also accelerated the recovery of brain electroencephalogram (EEG) after microwave exposure, indicating that astragaloside could promote the normalization of neuronal functions. In conclusion, astragaloside protected the morphological structures and restored acetylcholine level in rat hippocampus, which could improve brain functions via normalizing brain EEG. Therefore, astragaloside might be a promising candidate to treat microwave-induced injuries of central nervous system (CNS). [ABSTRACT FROM AUTHOR]

Copyright of Asian Journals of Ecotoxicology is the property of Gai Kan Bian Wei Hui and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Objective To investigate the effect of intraperitoneal injection of naloxone on learning and memory ability and autophagy in hippocampal CAl area of rats with subarachnoid hemorrhage (SAH). Methods Thirty-six male Sprague- Dawley rats were randomly divided into the sham operation group (sham group), SAH group, and SAH + naloxone group (naloxone group). The rat models of SAH were established by internal carotid artery puncture. In the sham operation group, we only penetrated the core into the skull along the blood vessel, but did not pierce the blood vessel. After successful modeling, the rats in the naloxone group were given naloxone injection (1 m/kg body weight) intraperitoneally, once/ 12 h. The rats in the sham operation group and the SAH group were given an equal amount of normal saline through intraperitoneal injection. At 24 hours after surgery, the shuttle box text was performed, and we compared the times of escape to safe area and the numbers of escape to safe area in the rats of three groups. Then the rats were sacrificed and hippocampus tissues were taken. The nerve cell morphology was observed by HE staining, immunohistochemistry was used to detect the number of Beclin-1 andL C3- II positive cells, and Western blotting to detect the expression of autophagy-specific markers Beclin-1 andL C3- II protein. Results Compared with the sham group, the time of escape to safe area was prolonged (P < 0. 05), and the number of escape to safe area was reduced in the SAH group (P < 0. 05). Compared with the SAH group, the time of escape to safe area was shorter (P < 0. 05), and the number of escape to safe area increased in the naloxone 停oup (P <0. 05) . HE staining showed that compared with the sham group, the number of normal morphology of hippocampal nerve cells decreased in the SAH group (P <0. 05) . Compared with the SAH group, the number of normal morphology of hippocampal nerve cells increased in the naloxone group (P <0. 05) . Compared with the sham group, the number of Beclin-1 and LC3-II positive cells increased in the SAH group ( P < 0. 05) . Compared with the SAH group, Beclin-1 and LC3-II positive cells increased in the naloxone group (all P < 0. 05) . Compared with the sham group, the expression of Beclin- 1 and LO-II protein increased in the SAH group (both P < 0. 05) . Compared with the SAH group, the expression of Beclin- 1 and LO-II protein increased in the naloxone group ( both P <0. 05) . Conclusion Naloxone can improve the learning and memory ab山ty, enhance autophagy in hippocampus of SAH rats, and reduce nerve cell damage in rats [ABSTRACT FROM AUTHOR]

This study aimed to investigate the effects of prenatal and lactational methcathinone exposure on the development and the learning and memory abilities of rat offspring using a Sprague-Dawley rat model. Pregnant and lactating rats were administered a consecutive daily dose of methcathinone (0.37 mg/kg) or an equivalent volume of saline by injection on gestational days 7–20 and postnatal days 2–15, respectively. The physical development and neurobehavioral test results of rat pups were recorded throughout the lactation period. Morris water maze (MWM) and novel object recognition (NOR) tests were performed from postnatal day 35 to day 42 to assess the learning and memory abilities of rat offspring in adolescence. The occurrence of hair growth and developments in neurological reflexes, such as improvements in limb grasp, righting reflex, and gait, were delayed in pups after perinatal methcathinone exposure compared with that in the control. Results from MWM and NOR tests indicate that perinatal methcathinone exposure induced deficits in spatial memory, learning ability, and novel object exploration in the adolescent offspring compared with that in the control. The impairment of spatial learning and memory was greater in the prenatal exposure group, while the impairment of novel object exploration was greater in the lactational exposure group. These data show that the prenatal and lactational methcathinone exposure induced the delay of physical and neurological reflex development and impaired learning and memory in rat offspring. [ABSTRACT FROM AUTHOR]

To investigate the effect of intraperitoneal injection of high-dose propofol (PPF) on learning and memory ability of Alzheimer 's disease (AD) model rats and to explore its mechanism. Methods AD model rats were established by intraperitoneal injection of D-galactose (D-gal) and gavage of aluminum trichloride (A1Cl3 ). They were randomly divided into the model group, donepezil group, low-dose PPF group, and high-dose PPF group. AD model rats in the donepezil group was intraperitoneally injected with donepezil, the low-dose PPF group with 50 mg/kg PPF, the high-dose PPF group with 100 mg/kg PPF, and the model group with equal volume of normal saline. Six normal SD rats were selected as the control group. Morris water maze test was used to evaluate learning and memory ability of rats in each group; Western blotting was used to detect β-amyloid protein (Aβ protein) and phosphorylated NF-KB (p- NF-KB) protein in hippocampus of rats in each group; colorimetric method was used to detect AchE activity in hippocampus of rats in each group; ELISA was used to detect IL-1 β, IL-6 and TNF-a protein in hippocampus of rats in each group. Results Compared with the control group, the learning and memory ability decreased, Aβ protein increased, AchE activity increased, p-NF-KB, IL-1β, IL--6 and TNF-a protein levels increased in the model group. Compared with the model group, the learning and memory ability increased, Aβ protein decreased, AchE activity decreased, and the levels of p-NF-KB, IL-1 β, IL- 6, and TNF-a protein decreased in the donepezil group, the low-dose PPF group, and the high-dose PPF group; there was no difference between the high-dose PPF group and donepezil group, and both of them were higher than the low-dose PPF group. Conclusions lntraperitoneal injection of high-dose PPF can significantly improve the learning and memory ability of AD model rats. The mechanism may be related to the inhibition of Aβ protein deposition in hippocampus, the enhancement of cholinergic function, the inhibition of NF-KB protein phosphorylation, and the reduction of inflammatory response in the brain. [ABSTRACT FROM AUTHOR]

Copyright of Practical Pharmacy & Clinical Remedies is the property of Editorial Department of Practical Pharmacy & Clinical Remedies and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

The aim of this study was to investigate the anti-ageing effect of Yisui moxibustion on regulating the klotho protein and insulin (INS)/IGF-1 signalling cascade in d-galactose mice. Sixty male Kunming mice were randomly divided into five groups after the Morries test: the normal sodium, model, moxa cone moxibustion 1 and 2, and sham groups. The treatment and model were given d-galactose injection for 70 days, while mice in the normal sodium group were injected the same dosage of normal sodium. From day 13 after the first injection, the three treatment groups were treated every day for 58 days. The INS and klotho in the cerebral tissues were measured. p-Akt, p-FoxO3a, Klotho, SOD2 expression were observed immunohistochemically. The escape latency of mice in the model and sham were significantly prolonged, and the spanning original platform times were significantly decreased compared with the normal sodium and moxa cone moxibustion 1 and 2 (p < 0.01). The content of INS and klotho in the model was significantly lower than the normal sodium, moxa cone moxibustion 1 and 2 (p < 0.01). Compared with the model and sham, p-Akt and p-FoxO3a expression in moxa cone moxibustion 1 and 2 were markedly decreased (p < 0.05), and the expressions of klotho and SOD2 were significantly increased (p < 0.05) in hippocampal CA1. Yisui moxibustion could exert the antioxidative effect on klotho protein, which negatively regulated the insulin signalling pathway and its downstream elements in cerebral tissue and hippocampal CA1, so as to enhance learning and memory capacities, delay brain ageing. [ABSTRACT FROM AUTHOR]

Objective To observe the effects of dexmedetomidine (Dex) preconditioning on apoptosis of hippocampal neurons in young and adult rats with sevoflurane inhalation during neonatal period. Methods Sixty neonatal male rats were randomly divided into three group; the sevoflurane group (group S), preconditioning with dexmedetomidine and sevoflurane group (group Dex), and control group (group C), with 20 rats in each group. Rats in the group S were intraperitoneally injected with 3 miykg saline before inhaling sevoflurane for 4 h on day 7, 14 and 21; 20 μg/kg Dex dissolved in 3 mL/kg saline was injected intraperitoneally into animals in the group Dex before 4-hour sevoflurane inhalation at the same time points. Rats in the group C inhaled carrier gas for 4 h after injecting 3 miykg saline. The level of neuronal apoptosis and the expression of cleaved-Caspase-3 in hippocampus were investigated at juvenile (37 days old) and adult period (97 days old). Results At juvenile and adult stage, the number of apoptotic neurons and the expression of cleaved Caspase-3 in the group S were higher than those in the group C and group Dex (both P <0.01). Among the three group, there was no significant difference between juvenile stage and adult stage in terms of the number of apoptotic neurons and the expression of cleaved Caspase-3 (all P >0.05). Conclusion Dex preconditioning can reduce the neuronal apoptosis induced by neonatal sevoflurane inhalation at the juvenile and adult stage, thereby protecting the brain tissues. [ABSTRACT FROM AUTHOR]

Objective To investigate the effect of Xingnaojing injection on learning and memory ability and autophagy-related protein expression of hippocampus nerve cells in rats with subarachnoid hemorrhage(SAH). Methods Thirtysix rats were randomly divided into the sham operation group, model group and Xingnaojing group, with 12 rats in each group. The SAH rat models were made by carotid puncture; in the sham operation group, we only penetrated the core into the skull along the blood vessel, but did not pierce the blood vessel. After successful modeling, rats in the Xingnaojing group were given intracerebroventricular injection of Xingnaojing 2 m L, 1 time/12 h; rats in the sham operation group and model group were given the same amount of normal saline. The shuttle box training was performed at 24 h after surgery, and we compared the time of avoidance reaction and the times of avoidance reaction in three groups. Then the rats were sacrificed and hippocampus were taken, we observed the nerve cell morphology by HE staining, using immunohistochemistry to detect the number of Beclin-1 and LC3II positive cells, and Western blotting to detect the expression of autophagy-specific markers Beclin-1 and LC3II protein. Results Compared with the sham operation group, the time of avoidance reaction was prolonged, and the times of avoidance decreased in the model group(both P<0. 05). Compared with the model group, the time of avoidance reaction was shortened, and the times of avoidance increased in the model group(both P <0. 05). Compared with the sham operation group, the number of hippocampal nerve cells with normal morphology decreased in the model group(P<0. 05). Compared with the model group, the number of hippocampal nerve cells with normal morphology increased in the Xingnaojing group(P<0. 05). Compared with the sham operation group, the number of Beclin-1 and LC3II positive cells increased in the model group, and the Xingnaojing group was higher than the model group(all P< 0. 05). Compared with the sham operation group, the expression of Beclin-1 and LC3II protein increased in the model group(both P<0. 05). Compared with the model group, the expression of Beclin-1 and LC3II protein increased in Xingnaojing group(both P<0. 05). Conclusion Xingnaojing can improve the learning and memory ability of SAH rats and protect brain nerve function, and its mechanism may be related to the activation of autophagy-related protein expression in hippocampus of SAH rats. [ABSTRACT FROM AUTHOR]

Brain glucose hypometabolism is a significant manifestation of Alzheimer's disease (AD). 27-hydroxycholesterol (27-OHC) and the gut microbiota have been recognized as factors possibly influencing the pathogenesis of AD. This study aimed to investigate the link between 27-OHC, the gut microbiota, and brain glucose uptake in AD. Here, 6-month-old male C57BL/6 J mice were treated with sterile water or antibiotic cocktails, with or without 27-OHC and/or 27-OHC synthetic enzyme CYP27A1 inhibitor anastrozole (ANS). The gut microbiota, brain glucose uptake levels, and memory ability were measured. We observed that 27-OHC altered microbiota composition, damaged brain tissue structures, decreased the 2-deoxy-2-[18 F] fluorodeoxyglucose (18F-FDG) uptake value, downregulated the gene expression of glucose transporter type 4 (GLUT4), reduced the colocalization of GLUT1/glial fibrillary acidic protein (GFAP) in the hippocampus, and impaired spatial memory. ANS reversed the effects of 27-OHC. The antibiotic-treated mice did not exhibit similar results after 27-OHC treatment. This study reveals a potential molecular mechanism wherein 27-OHC-induced memory impairment might be linked to reduced brain glucose uptake, mediated by the gut microbiota. [Display omitted] • 27-OHC affects gut microbiota composition and induces gut microbiota dysbiosis. • 27-OHC decreases brain glucose uptake and induces memory impairment of mice. • 27-OHC did not decrease brain glucose uptake in microbiota-depleted mice. • GLUT1 and GLUT4 are important factors in the regulation of brain glucose uptake. [ABSTRACT FROM AUTHOR]

: Our previous study found that hyperbaric oxygen (HBO) attenuated cognitive impairment in mice induced by cerebral ischemia-reperfusion injury (CIRI). However, its mechanism of action is not fully understood. In this study, we aimed to establish a rat model of cerebral ischemia-reperfusion, explore the possible role of ferroptosis in the pathogenesis of CIRI, and observe the effect of HBO on ferroptosis-mediated CIRI. : Sprague Dawley (SD) rats were randomly divided into control, model, Ferrostatin-1 (Fer-1), HBO and Fer-1+ HBO groups. Morris water maze, myelin basic protein (MBP) and β-tubulin immunoreactivity were assessed to evaluate the neuroprotective effects of HBO on cerebral ischemia reperfusion injury. Ferroptosis were examined to investigate the mechanism underlying the effects of HBO. : Our result showed that Fer-1 and HBO improved learning and memory ability in the navigation trail and probe trail of the Morris water maze and increased MBP and β-tubulin immunoreactivity of the cortex in the model rats. The levels of ferritin, malondialdehyde (MDA) and glutathione (GSH) in the serum were also reversed by Fer-1 and HBO treatment. Mitochondrial cristae dissolution and vacuolization were observed in the model group by transmission electron microscopy and these conditions were improved in the Fer-1 and HBO groups. Furthermore, Fer-1 and HBO treatment reversed Prostaglandin-Endoperoxide Synthase 2 (PTGS2), Iron Responsive Element Binding Protein 2 (IREB2), acyl-CoA synthetase long chain family member 4 (ACSL4) and Solute Carrier Family 7 Member 11 (SLC7A11) mRNA levels and Transferrin Receptor 1 (TFR1), ferritin light chain (FTL), ferritin heavy chain 1 (FTH1), glutathione peroxidase 4 (GPX4), Nuclear factor E2-related factor 2 (Nrf2), lysophosphatidylcholine acyltransferase 3 (LPCAT3), c-Jun N-terminal kinase (JNK), phosphorylated c-Jun N-terminal kinase (P-JNK) phosphorylated Extracellular signal-regulated protein kinase (P-ERK) and mitogen-activated protein kinase/extracellular signal-regulated kinase (MEK) protein levels. The above changes were more pronounced in Fer-1+ HBOGroup. : The results of the present study indicated that HBO improves cerebral ischemia-reperfusion injury in rats, which may be related to inhibition of ferroptosis. This also means that ferroptosis may become a new target of HBO against CIRI. [ABSTRACT FROM AUTHOR]

Objective:To observe the effect of electro-acupuncture (EA) at Changqiang (GV1) acupoint on the learning and memory ability and hippocampal CA1 cellular apoptosis in rats with vascular dementia (VD).Methods:Sixty male SD rats according to the Morris water maze test were divided into three groups: 9 rats for blank control group, 9 rats for sham-operated group and 42 rats for surgical control group. Rats of VD models were established by 2 vessels obstruction (2-VO), 27 rats were selected from the surgical control group and divided into three groups: 9 rats for model group, 9 rats for EA treatment group and rest 9 rats for the non-acupoint EA control group. After the treatment, the water maze test and the TUNEL test were examined.Results:Compared with the model group, the escape latent period and the CA1 apoptosis of the blank control group and the EA treatment group were apparently shorter (PPPP

Background: Our previous research has shown that prenatal methcathinone exposure affects the neurodevelopment and neurobehavior of adolescent offspring, but the study on whether these findings continue into adulthood is limited., Objective: This study aims to explore the effects of prenatal methcathinone exposure on anxiety-like behavior, learning and memory abilities, as well as serum 5-hydroxytryptamine and dopamine concentrations in adult offspring., Methods: Pregnant rats were injected daily with methcathinone between the 7th and 20th days of gestation. The neurobehavioral performance of both male and female adult offspring rats was evaluated by neurobehavioral tests, including open-field tests, Morris water maze (MWM) tests, and novel object recognition (NOR) tests. The levels of 5-hydroxytryptamine and dopamine concentration in rat serum were detected by ELISA., Results: Significant differences were found in the length of center distance and time of center duration in the open-field test, as well as the times of crossing the platform in the MWM test, between the prenatal methcathinone exposure group and the control group. Results of the NOR test showed that adult offspring rats exposed to methcathinone need more time to discriminate the novel object. No gender differences were detected in the neurobehavioral tests. The serum concentrations of 5-hydroxytryptamine and dopamine in rats exposed to methcathinone prenatally were lower than that in the control group, and the serum dopamine concentration was independent of gender in each group., Conclusion: Prenatal methcathinone exposure affects the neurological behavior in adult offspring, and 5-hydroxytryptamine and dopamine might be involved in the process., (Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.)

In our previous study, chromium malate is beneficial for type 2 diabetic rats in control glycometabolism and lipid metabolism. The present study was designed to observe the chronic toxicity, lipid metabolism, learning and memory ability, and related enzymes of chromium malate in rats during the year. The results showed that pathological, toxic, feces, and urine of chromium malate (at daily doses of 10.0, 15.0, and 20.0 μg Cr/kg bm) did not change measurably. Chromium malate (at daily doses of 15.0 and 20.0 μg Cr/kg bm) could significantly reduce the levels of total cholesterol (TC), LDL, and triglyceride (TG), and increase the level of HDL in male rats compared to control group and chromium picolinate group. Significant escalating trends of the escape latency and swimming speed (Morris water maze test), and the original platform quadrant stops, residence time, and swimming speed (Space exploration test) in male rats of chromium malate groups were obtained. The SOD, GSH-Px, and TChE activities of chromium malate (at daily doses of 15.0 and 20.0 μg Cr/kg bm) were enhanced significantly in male rats compared with those of the normal control group and chromium picolinate group. Glycometabolism and related enzymes had no significant changes compared to normal control group and chromium picolinate group. These results indicated that long-term chromium malate supplementation did not cause measurable toxicity at daily doses of 10.0, 15.0, and 20.0 μg Cr/kg bm and could improve dyslipidemia and learning and memory deficits. [ABSTRACT FROM AUTHOR]

With the rapid development of ultra-high-voltage direct-current (UHVDC) transmission, the strength of environmental static electric field (SEF) around UHVDC transmission lines increased substantially, which has aroused widely public attention on the potential health effects of SEF. In this study, the effect of SEF exposure on learning and memory ability was investigated. Institute of Cancer Research mice were exposed to 56.3 kV/m SEF for a short term (7 days) or long term (49 days). Behaviors in the Morris water maze (MWM) test, hippocampal neurotransmitter contents, and oxidative stress indicators were examined. Results showed that short-term SEF exposure significantly prolonged escape latency and decreased the number of platform-site crossovers, as well as decreased the time spent in the target quadrant in the MWM test. Meanwhile, serotonin level and the ratio of glutamate level to γ-aminobutyric acid level changed significantly. Besides, malondialdehyde content and glutathione peroxidase activity increased significantly, while superoxide dismutase activity decreased significantly. After long-term SEF exposure, all indices above showed no significant differences between the SEF and sham exposure groups. These data indicated that short-term exposure to 56.3 kV/m SEF could cause abnormal neurotransmitter levels and oxidative stress in the hippocampus, which led to the decline in learning and memory ability. Under the condition of long-term exposure, the SEF-induced disturbances in neurotransmitter contents and redox balance were offset by the compensatory responses of mice, and thus, the learning and memory ability returned to normal level. The temporary and reversible decline in learning and memory ability was only a common biological effect of SEF rather than a health hazard. [ABSTRACT FROM AUTHOR]

Ｏｂｊｅｃｔｉｖｅ　Ｔｏ ｏｂｓｅｒｖｅ ｔｈｅ ｌｅａｒｎｉｎｇ ａｎｄ ｍｅｍｏｒｙ ａｂｉｌｉｔｙ ａｎｄ ｓｐａｔｉａｌ ｅｘｐｌｏｒａｔｉｏｎ ａｂｉｌｉｔｙ，ｓｅｒｕｍ ｉｎｆｌａｍｍａｔｏｒｙ ｆａｃｔｏｒｓ，ａｎｄ ｂｒａｉｎ ｔｉｓｓｕｅ ｎｅｕｒｏｅｎｚｙｍｅ ａｃｔｉｖｉｔｙ ｏｆ ＳＤ ｍａｌｅ ｒａｔｓ ａｆｔｅｒ ｄｒｉｎｋｉｎｇ ７２-ｗｅｅｋ Ｍｉａｏ ｍｅｄｉｃｉｎｅ ａｓｐａｒａｇｕｓ ｄｅｃｏｃｔｉｏｎ． Ｍｅｔｈｏｄｓ　Ｅｉｇｈｔｅｅｎ ｒａｔｓ ｗｅｒｅ ｄｉｖｉｄｅｄ ｉｎｔｏ ｔｈｅ ａｓｐａｒａｇｕｓ ｇｒｏｕｐ，ａｇｉｎｇ ｇｒｏｕｐ，ａｎｄ ｃｏｎｔｒｏｌ ｇｒｏｕｐ ｗｉｔｈ ６ ｒａｔｓ ｉｎ ｅａｃｈ ｇｒｏｕｐ． Ｒａｔｓ ｉｎ ｔｈｅ ａｓｐａｒａｇｕｓ ｇｒｏｕｐ ｗｅｒｅ ｆｒｅｅ ｔｏ ｄｒｉｎｋ １２ ｇ／ Ｌ ｏｆ ａｓｐａｒａｇｕｓ ｄｅｃｏｃｔｉｏｎ ｆｏｒ ７２ ｗｅｅｋｓ （ａｃｃｏｒｄｉｎｇ ｔｏ ７２ ｗｅｅｋｓ ｏｆ ｍｅｄｉ- ｃａｌ ｌａｂｏｒａｔｏｒｙ ｚｏｏｌｏｇｙ，ｗｈｉｃｈ ｉｓ ｅｑｕｉｖａｌｅｎｔ ｔｏ ５０ ｔｏ ５５ ｙｅａｒｓ ｏｌｄ，ｔｈｅ ｏｌｄ ａｇｅ ｏｆ ｒａｔｓ），ｔｈｅ ｒａｔｓ ｉｎ ｔｈｅ ａｇｉｎｇ ｇｒｏｕｐ ｗｅｒｅ ｆｒｅｅ ｔｏ ｄｒｉｎｋ ｗａｔｅｒ ｆｏｒ ７２ ｗｅｅｋｓ，ｒａｔｓ ｉｎ ｔｈｅ ｃｏｎｔｒｏｌ ｇｒｏｕｐ ｗｅｒｅ ｆｒｅｅ ｔｏ ｄｒｉｎｋ ｗａｔｅｒ ｆｏｒ ６ ｗｅｅｋｓ． Ｔｈｅ Ｍｏｒｒｉｓ ｗａｔｅｒ ｍａｚｅ ｔｅｓｔ ｗａｓ ｕｓｅｄ ｔｏ ｅｖａｌｕａｔｅ ｔｈｅ ｌｅａｒｎｉｎｇ ａｎｄ ｍｅｍｏｒｙ ａｎｄ ｓｐａｃｅ ｅｘｐｌｏｒａｔｉｏｎ ａｂｉｌｉｔｙ ｉｎ ｒａｔｓ． Ｕｓｉｎｇ ｅｎｚｙｍｅ-ｌｉｎｋｅｄ ｉｍｍｕｎｏｓｏｒｂｅｎｔ ａｓｓａｙ ｔｏ ｄｅｔｅｃｔ ｔｈｅ ｓｅｒｕｍ ＩＬ-１，ＩＬ-６，ａｎｄ ａｃｅｔｙｌｃｈｏｌｉｎｅｓｔｅｒａｓｅ ｉｎ ｂｒａｉｎ ｔｉｓｓｕｅ （ＡｃｈＥ）ａｎｄ ｃｈｏｌｉｎｅ ａｃｅｔｙｌｔｒａｎｓｆｅｒａｓｅ （ＣｈＡＴ）ａｃ- ｔｉｖｉｔｙ． Ｒｅｓｕｌｔｓ　Ｃｏｍｐａｒｅｄ ｗｉｔｈ ｔｈｅ ｃｏｎｔｒｏｌ ｇｒｏｕｐ，ｏｎ ｄａｙ １-４，ｔｈｅ ｗａｔｅｒ ｍａｚｅ ｌａｔｅｎｃｙ ｏｆ ｒａｔｓ ｏｆ ｔｈｅ ａｓｐａｒａｇｕｓ ｇｒｏｕｐ ａｎｄ ａｇｉｎｇ ｇｒｏｕｐ ｗａｓ ｌｏｎｇ （Ｐ ＜０． ０５）． Ｃｏｍｐａｒｅｄ ｗｉｔｈ ｔｈｅ ａｇｉｎｇ ｇｒｏｕｐ，ｏｎ ｔｈｅ ４ｔｈ ｄａｙ，ｔｈｅ ｗａｔｅｒ ｍａｚｅ ｌａｔｅｎｃｙ ｏｆ ｒａｔｓ ｗａｓ ｓｈｏｒｔ ｉｎ ｔｈｅ ａｓｐａｒａｇｕｓ ｇｒｏｕｐ （Ｐ ＜０． ０５）． Ｃｏｍｐａｒｅｄ ｗｉｔｈ ｔｈｅ ｃｏｎｔｒｏｌ ｇｒｏｕｐ，ｏｎ ｄａｙ ２-４，ｔｈｅ ｓｗｉｍｍｉｎｇ ｄｉｓｔａｎｃｅ ｏｆ ｒａｔｓ ｉｎ ｔｈｅ ａｓ- ｐａｒａｇｕｓ ｇｒｏｕｐ ａｎｄ ａｇｉｎｇ ｇｒｏｕｐ ｗａｓ ｌｏｎｇｅｒ （Ｐ ＜０． ０５）． Ｏｎ ｄａｙ ５，ｃｏｍｐａｒｅｄ ｗｉｔｈ ｔｈｅ ｃｏｎｔｒｏｌ ｇｒｏｕｐ，ｔｈｅ ｔｉｍｅ ｏｆ ｆｉｒｓｔ ｃｒｏｓｓ- ｉｎｇ ｔｈｅ ｐｌａｔｆｏｒｍ ｏｆ ｔｈｅ ｒａｔｓ ｉｎ ｔｈｅ ａｓｐａｒａｇｕｓ ｇｒｏｕｐ ｗａｓ ｌｏｎｇｅｒ，ａｎｄ ｔｈｅ ｎｕｍｂｅｒ ｏｆ ｃｒｏｓｓｉｎｇ ｐｌａｔｆｏｒｍ ｗａｓ ｌｅｓｓ；ｔｈｅ ｔｉｍｅ ｏｆ ｆｉｒｓｔｃｒｏｓｓｉｎｇ ｔｈｅ ｐｌａｔｆｏｒｍ ｉｎ ｔｈｅ ａｇｉｎｇ ｇｒｏｕｐ ｗａｓ ｌｏｎｇｅｒ，ａｎｄ ｔｈｅ ｎｕｍｂｅｒ ｏｆ ｃｒｏｓｓｉｎｇ ｐｌａｔｆｏｒｍ ｗａｓ ｌｅｓｓ，ｗｉｔｈ ａ ｓｈｏｒｔｅｒ ｔｉｍｅ ｏｆ ｃｒｏｓｓｉｎｇ ｔｈｅ ｐｌａｔｆｏｒｍ （ａｌｌ Ｐ ＜０． ０５）． Ｃｏｍｐａｒｅｄ ｗｉｔｈ ｔｈｅ ａｇｉｎｇ ｇｒｏｕｐ，ｏｎ ｔｈｅ ｆｉｆｔｈ ｄａｙ，ｔｈｅ ｔｉｍｅ ｏｆ ｆｉｒｓｔ ｃｒｏｓｓｉｎｇ ｔｈｅ ｐｌａｔ- ｆｏｒｍ ｏｆ ｔｈｅ ｒａｔｓ ｉｎ ｔｈｅ ａｓｐａｒａｇｕｓ ｇｒｏｕｐ ｗａｓ ｓｈｏｒｔｅｒ，ａｎｄ ｔｈｅ ｎｕｍｂｅｒ ｏｆ ｃｒｏｓｓｉｎｇ ｐｌａｔｆｏｒｍ ｗａｓ ｍｏｒｅ （ａｌｌ Ｐ ＜ ０． ０５）． Ｃｏｍ- ｐａｒｅｄ ｗｉｔｈ ｔｈｅ ｃｏｎｔｒｏｌ ｇｒｏｕｐ，ｔｈｅ ｌｅｖｅｌｓ ｏｆ ｓｅｒｕｍ ＩＬ-１ ａｎｄ ＩＬ-６ ｉｎ ｔｈｅ ａｓｐａｒａｇｕｓ ａｎｄ ａｇｉｎｇ ｇｒｏｕｐｓ ｗｅｒｅ ｉｎｃｒｅａｓｅｄ （ｂｏｔｈ Ｐ ＜ ０． ０５）． Ｃｏｍｐａｒｅｄ ｗｉｔｈ ｔｈｅ ａｇｉｎｇ ｇｒｏｕｐ，ｔｈｅ ｌｅｖｅｌｓ ｏｆ ｓｅｒｕｍ ＩＬ-１ ａｎｄ ＩＬ-６ ｉｎ ｔｈｅ ａｓｐａｒａｇｕｓ ｇｒｏｕｐ ｗｅｒｅ ｌｏｗｅｒ （ｂｏｔｈ Ｐ ＜ ０． ０５）． Ｃｏｍｐａｒｅｄ ｗｉｔｈ ｔｈｅ ｃｏｎｔｒｏｌ ｇｒｏｕｐ，ｔｈｅ ａｃｔｉｖｉｔｉｅｓ ｏｆ ＡｃｈＥ ｉｎ ｔｈｅ ａｓｐａｒａｇｕｓ ｇｒｏｕｐ ａｎｄ ａｇｉｎｇ ｇｒｏｕｐ ｗｅｒｅ ｅｎｈａｎｃｅｄ， ａｎｄ ＣｈＡＴ ａｃｔｉｖｉｔｙ ｗａｓ ｄｅｃｒｅａｓｅｄ （ｂｏｔｈ Ｐ ＜０． ０５）． Ｃｏｍｐａｒｅｄ ｗｉｔｈ ｔｈｅ ａｇｉｎｇ ｇｒｏｕｐ，ｔｈｅ ａｃｔｉｖｉｔｙ ｏｆ ＡｃｈＥ ｗａｓ ｗｅａｋｅｎｅｄ ａｎｄ ｔｈｅ ＣｈＡＴ ａｃｔｉｖｉｔｙ ｗａｓ ｉｎｃｒｅａｓｅｄ ｉｎ ｔｈｅ ａｓｐａｒａｇｕｓ ｇｒｏｕｐ （ｂｏｔｈ Ｐ ＜ ０． ０５）． Ｃｏｎｃｌｕｓｉｏｎ　Ｔｈｅ ｌｅａｒｎｉｎｇ ａｎｄ ｍｅｍｏｒｙ ａｎｄ ｓｐａｃｅ ｅｘｐｌｏｒａｔｉｏｎ ａｂｉｌｉｔｙ，ｔｈｅ ｌｅｖｅｌ ｏｆ ｓｅｒｕｍ ｉｎｆｌａｍｍａｔｏｒｙ ｆａｃｔｏｒｓ，ａｎｄ ｂｒａｉｎ ｔｉｓｓｕｅ ｎｅｕｒｏｅｎｚｙｍｅ ａｃｔｉｖｉｔｙ ｏｆ ＳＤ ｍａｌｅ ｒａｔｓ ａｆ- ｔｅｒ ｄｒｉｎｋｉｎｇ ７２-ｗｅｅｋ Ｍｉａｏ ｍｅｄｉｃｉｎｅ ａｓｐａｒａｇｕｓ ｄｅｃｏｃｔｉｏｎ ａｒｅ ｉｍｐｒｏｖｅｄ． [ABSTRACT FROM AUTHOR]

The aim of this study is to investigate the effect of vitamin D (VD) on the learning and memory ability of fetal growth restriction (FGR) rat and the expression of NMDA receptor in hippocampus. The FGR models of rat were established through passive smoking, and divided into two groups randomly, i.e. the control group and the observation group. Rats were fed regular diet with the addition of VD in the observation group. The serum level of 25(OH)-D3 was assayed in both groups of the rats at different time points using ELISA, and the learning and memory ability of rat aged 30 days were evaluated using Morris water maze and passive avoidance test. In addition, we also compared the brain weight of rats at different age and detected the mRNA expression of NRI subunit of NMDA receptor of hippocampus of rats aged 30 days using quantitative RT-PCR. After 7 days, the serum level of 25(OH)D3 in rats of the observation group was significantly higher than that of the control group (P<0.05); during the Morris water maze, we found no significant difference in comparison of the latency between the two groups in the first 2 days (P>0.05), but from the 3rd day, the latency of the observation group was shorter than that in the control group (P<0.05); in the passive avoidance test, no significant difference was identified when comparing the electric shock times between the two groups in the first 2 days, but from the 3rd day, the electric shock times in the observation group were significantly lower than those in the control group (P<0.05); the brain weight of rats in the observation group on the 1st, 7th and 14th day were all lower than those in the control group (P<0.05), but the comparison of brain weight at 21st and 30th day showed no significant difference (P>0.05) between the two groups. We also found that the mRNA and protein expression of NRI subunit of NMDA receptor in hippocampus was significantly higher in the observation group than in the control group (P<0.05). VD can increase the learning and memory ability of FGR rats, significantly ameliorating the cognitive dysfunction of FGR rat and improving the learning and memory ability of rats, which may be related to the upregulation of NRI subunit of NMDA receptor. [ABSTRACT FROM AUTHOR]

[Display omitted] • Physical therapy in the form of olfactory stimulation holds promise as a new adjunct to cognitive disorders. • Five essential oils with homologous food and medicine were used as physiotherapy in this study. • Network pharmacological prediction combined with molecular biology to verify anti-AD targets. • Olfactory stimulation may alleviate cognitive impairment in AD by activating antioxidant stress responses and improving synaptic function. High levels of Aβ accumulation leads to hippocampal damage, resulting in impaired oxidative stress responses and synaptic function, and ultimately cognitive impairment. Here, we investigated the effects of olfactory stimuli on Aβ1-42-induced AD models using an essential oil containing drug-food congeners. Through behavioral experiments, we found that the learning and memory ability of rats was affected to a certain extent after the injection of Aβ1-42 into the lateral ventricle, and the olfactory stimulation could improve the cognitive impairment caused by Aβ1-42. In addition, we applied network pharmacology to predict multiple possible anti-AD mechanisms based on the composition of essential oils used as olfactory stimuli. We selected the effects of olfactory stimuli on oxidative stress response and synaptic function, and found that Nrf2 signaling pathway and NMDAR/PSD95/nNOS signaling pathway were activated. Our results suggest that olfactory stimulation holds promise as a treatment for cognitive impairment. [ABSTRACT FROM AUTHOR]

Objectives: To observe the effect of electroacupuncture (EA) on microglia (MG), Janus kinase-2 (JAK2) and signal transducer and activator of transcription-3 (STAT3) in hippocampal CA1 region of Alzheimer's di-sease (AD) rats, so as to explore its mechanisms in the treatment of AD., Methods: Thirty-six male SD rats were randomly divided into sham operation, model and EA groups, with 12 rats in each group. The AD rat model was established by intraperitoneal injection of D-galactose combined with intrahippocampal injection of aggregated Aβ 25-35 . The rats in the EA group were given EA (2 Hz/20 Hz, 2 mA) at "Baihui"(GV20) and"Shenting"(GV24) for 30 min, once daily, 6 days a week for 4 weeks. Morris water maze test was used to detect the learning and memory ability and spatial exploration ability of rats. HE staining was used to observe the pathological changes of hippocampus. The ultrastructure of hippocampal neurons was observed by transmission electron microscopy. The positive expression of MG marker io-nized calcium adaptor protein (Iba-1) in hippocampus was observed by immunofluorescence staining. The expression levels of serum inflammatory factor interferon-γ (IFN-γ) and transforming growth factor beta 1 (TGF-β1) were detected by ELISA. The mRNA expression levels of JAK2, STAT3, inducible nitric oxide synthase (iNOS) and arginase-1 (Arg-1) in hippocampal CA1 region were detected by real-time quantitative PCR. The protein and phosphorylation levels of JAK2 and STAT3 in hippocampal CA1 region were detected by Western blot., Results: Compared with the sham operation group, the escape latency of the model group was significantly prolonged ( P <0.01), and the number of crossing the original platform was significantly reduced ( P< 0.01), the positive expression of Iba-1 in CA1 region, the content of serum IFN-γ, the relative mRNA expressions of JAK2, STAT3 and iNOS, and the protein and phosphorylation levels of JAK2 and STAT3 were significantly increased ( P <0.01), while the content of serum TGF-β1 and the relative expression of Arg-1 mRNA were significantly decreased ( P <0.01). Compared with the model group, the escape latency of rats in the EA group was significantly shortened ( P <0.01), the number of crossing the original platform was significantly increased ( P <0.01), the positive expression of Iba1, the content of serum IFN-γ, the mRNA expressions of JAK2, STAT3 and iNOS, and the protein and phosphorylation levels of JAK2 and STAT3 were significantly decreased ( P <0.05, P <0.01), while the content of serum TGF-β1 and the expression of Arg-1 mRNA were significantly increased ( P <0.01). Moreover, pathological and ultrastructural observation showed a reduction in the number of hippocampal neurons, changement of nuclear morphology, dilation of intercellular space, and decreased number of mitochondria in the model group；these situations were relatively milder in the EA group., Conclusions: EA can improve the learning and memory function of AD rats, which may be associated with its functions in decreasing MG activities, and inhibiting the JAK2 / STAT3 signaling pathway in the hippocampus.

Objective: To observe the effects of moxa smoke through olfactory pathway on learning and memory ability in rapid aging (SAMP8) mice, and to explore the action pathway of moxa smoke., Methods: Forty-eight six-month-old male SAMP8 mice were randomly divided into a model group, an olfactory dysfunction group, a moxa smoke group and an olfactory dysfunction + moxa smoke group, with 12 mice in each group. Twelve age-matched male SAMR1 mice were used as the blank group. The olfactory dysfunction model was induced in the olfactory dysfunction group and the olfactory dysfunction + moxa smoke group by intraperitoneal injection of 3-methylindole (3-MI) with 300 mg/kg, and the moxa smoke group and the olfactory dysfunction + moxa smoke group were intervened with moxa smoke at a concentration of 10-15 mg/m 3 for 30 min per day, with a total of 6 interventions per week. After 6 weeks, the emotion and cognitive function of mice was tested by open field test and Morris water maze test, and the neuronal morphology in the CAI area of the hippocampus was observed by HE staining. The contents of neurotransmitters (glutamic acid [Glu], gamma-aminobutyric acid [GABA], dopamine [DA], and 5-hydroxytryptamine [5-HT]) in hippocampal tissue of mice were detected by ELISA., Results: The mice in the blank group, the model group and the moxa smoke group could find the buried food pellets within 300 s, while the mice in the olfactory dysfunction group and the olfactory dysfunction + moxa smoke group took more than 300 s to find them. Compared with the blank group, the model group had increased vertical and horizontal movements ( P <0.05) and reduced central area residence time ( P <0.05) in the open field test, prolonged mean escape latency on days 1-4 ( P <0.05), and decreased search time, swimming distance and swimming distance ratio in the target quadrant of the Morris water maze test, and decreased GABA, DA and 5-HT contents ( P <0.05, P <0.01) and increased Glu content ( P <0.05) in hippocampal tissue. Compared with the model group, the olfactory dysfunction group had increased vertical movements ( P <0.05), reduced central area residence time ( P <0.05), and increased DA content in hippocampal tissue ( P <0.05); the olfactory dysfunction + moxa smoke group had shortened mean escape latency on days 3 and 4 of the Morris water maze test ( P <0.05) and increased DA content in hippocampal tissue ( P <0.05); the moxa smoke group had prolonged search time in the target quadrant ( P <0.05) and increased swimming distance ratio, and increased DA and 5-HT contents in hippocampal tissue ( P <0.05, P <0.01) and decreased Glu content in hippocampal tissue ( P <0.05). Compared with the olfactory dysfunction group, the olfactory dysfunction + moxa smoke group showed a shortened mean escape latency on day 4 of the Morris water maze test ( P <0.05). Compared with the moxa smoke group, the olfactory dysfunction + moxa smoke group had a decreased 5-HT content in the hippocampus ( P <0.05). Compared with the blank group, the model group showed a reduced number of neurons in the CA1 area of the hippocampus with a disordered arrangement; the olfactory dysfunction group had similar neuronal morphology in the CA1 area of the hippocampus to the model group. Compared with the model group, the moxa smoke group had an increased number of neurons in the CA1 area of the hippocampus that were more densely packed. Compared with the moxa smoke group, the olfactory dysfunction + moxa smoke group had a reduced number of neurons in the CA1 area of the hippocampus, with the extent between that of the moxa smoke group and the olfactory dysfunction group., Conclusion: The moxa smoke could regulate the contents of neurotransmitters Glu, DA and 5-HT in hippocampal tissue through olfactory pathway to improve the learning and memory ability of SAMP8 mice, and the olfactory is not the only effective pathway.