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Aims The protective effects of Bacillus amyloliquefaciens (CCT7935), Bacillus subtilis (CCT7935), Bacillus licheniformis (CCT 7836), and Bacillus coagulans (CCT 0199) against lipopolysaccharide (LPS)-induced intestinal inflammation were investigated. Methods and results Male Swiss mice were assigned into six groups: control group, LPS group, LPS +  B. subtilis (CCT7935) group, LPS +    B. licheniformis (CCT 7836) group, LPS +    B. amyloliquefaciens (CCT7935) group, and LPS    + B. coagulans (CCT 0199) group. Each mouse of the groups Bacillus received 1 × 109 colony-forming units of Bacillus once daily by oral gavage during 30 days. Twenty-four hours after the last dose of Bacillus , all groups, except the control group, were intraperitoneally injected with LPS in the single dose of 15 mg kg−1. The mice were euthanized 24 h after the LPS administration. Histological alterations, myeloperoxidase activity, and nitrite levels were analyzed in the gut of mice and the inflammatory cytokines were analyzed in the gut and in the blood. The results demonstrate that the mice challenged with LPS presented the villi shortened and damaged, which were significantly protected by B. coagulans and B. amyloliquefaciens. Furthermore, all Bacillus tested were effective in preventing against the increase of myeloperoxidase activity, while B. amyloliquefaciens and B. subtilis prevented the increase of nitrite and IL-1β levels in the gut of mice induced with LPS was decreased only B. subtilis. LPS also elevated the IL-1 β, IL-6, and IL-10 levels in the blood, and these alterations were significantly suppressed by Bacillus , especially by B. subtilis. Conclusions The study suggests that the Bacillus investigated in this study might be effective therapeutic agents for preventing intestinal inflammation, because they decrease the inflammatory process an protect against tissue damage. [ABSTRACT FROM AUTHOR]

Folic acid (FA) supplementation is important during pregnancy to avoid malformations in the offspring. However, it is unknown if it can affect the offspring throughout their lives. To evaluate the offspring, female mother rats (dams) were separated into 5 groups: Four groups received the AIN-93 diet, divided into control and FA (5, 10, and 50 mg/kg), and an additional group received a FA-deficient diet, and the diet was performed during pregnancy and lactation. We evaluated the female offspring of these dams (at 2 and 18 months old). The aged offspring fed with FA-deficient diet presented habituation, spatial and aversive memory impairment and the FA maternal supplementation prevented this. The natural aging caused an increase in the TNF-α and IL-1β levels in the hippocampus from 18-month-old offspring. FA maternal supplementation was able to prevent the increase of these cytokines. IL-4 levels decreased in the prefrontal cortex from aged control rats and FA prevented it. FA deficiency decreased the levels of IL-4 in the hippocampus of the young offspring. In addition, natural aging and FA deficiency decreased brain-derived neurotrophic factor levels in the hippocampus and nerve growth factor levels in the prefrontal cortex and FA supplementation prevented it. Thus, the present study shows for the first time the effect of FA maternal supplementation on memory, cytokines, and neurotrophins in the aged offspring. [ABSTRACT FROM AUTHOR]

D-galactose (D-gal) is a carbohydrate widely distributed in regular diets. However, D-gal administration in rodents is associated with behavioral and neurochemical alterations similar to features observed in aging. In this regard, this study aimed to investigate the effects of D-gal exposure, in different periods, in rats’ brain regions’ activities of creatine kinase (CK) and tricarboxylic acid (TCA) cycle enzymes. Male adult Wistar rats received D-gal (100 mg/kg, gavage) for 1, 2, 4, 6 or 8 weeks. CK and TCA enzymes’ activities were evaluated in rats’ prefrontal cortex and hippocampus. In general, the results showed an increase in citrate synthase (CS) and succinate dehydrogenase (SDH) activities in animals treated with D-gal compared to the control group in the prefrontal cortex and hippocampus. Also, in the fourth week, the malate dehydrogenase (MD) activity increased in the hippocampus of rats that received D-gal compared to control rats. In addition, we observed an increase in the CK activity in the prefrontal cortex and hippocampus in the first and eighth weeks of treatment in the D-gal group compared to the control group. D-gal administration orally administered modulated TCA cycle enzymes and CK activities in the prefrontal cortex and hippocampus, which were also observed in aging and neurodegenerative diseases. However, more studies using experimental models are necessary to understand better the impact and contribution of these brain metabolic abnormalities associated with D-gal consumption for aging. [ABSTRACT FROM AUTHOR]

Background: Alzheimer's disease (AD) is a progressive neurodegenerative disease. The animal model of AD‐like dementia induced by the peptide β‐amyloid 1‐42 (Aβ1‐42) is widely used. However, the animals have to be anesthetized and no studies are evaluating which anesthetic causes less interference in this model. This study aimed to evaluate the interference of different anesthetics on behavioral and oxidative stress in a mice model of Aβ1‐42‐induced dementia. Method: Male and female BALB/c mice at 3‐ month‐old were used under three different protocols. Protocol 1 (inhalation): (1) 100% oxygen (isoflurane control); (2) artificial cerebrospinal fluid (ACSF) + isoflurane; (3) Aβ1‐42 + isoflurane. Protocol 2 (intraperitoneal): (1) saline; (2) ACSF + ketamine + xylazine; (3) ACSF + ketamine + dexmedetomidine; (4) Aβ1‐42 + ketamine + xylazine; (5) Aβ1‐42 + ketamine + dexmedetomidine. Protocol 3 (intraperitoneal): (1) saline; (2) ACSF + propofol; (3) Aβ1‐42 + propofol. After the anesthesia, mice were injected with Aβ1‐42 (400 pmol) free‐hand intracerebroventricular, then after 13 days, mice were submitted to the Y‐maze test (spatial memory), plus‐maze (anxiety), and open‐field (habituation memory); then, hippocampus were dissected to analysis. Result: Isoflurane per se (protocol 1) caused no memory impairment, but caused an anxiolytic effect in males, in addition, to increased sulfhydryl content in males. In protocol 2, ACSF + ketamine + xylazine induced spatial memory impairment in males and habituation memory impairment in females; the anesthetics of protocol 2 increased 2',7' dichlorodihydrofluorescein (DCF) levels in females, and ACSF + ket + dex reduced levels of glutathione (GSH) in males. In protocol 3, propofol per se caused an anxiolytic effect in males and increased DCF levels in males and females, increased superoxide dismutase activity in males, and reduction in females, in addition, increased sulfhydryl content in males. Conclusion: All anesthetic protocols evaluated caused alterations in the behavior and/or oxidative stress parameters; however, isoflurane seems to cause less interference in the animal model, followed by propofol. Protocol 3 seems to cause more interference, including in the Y‐maze (spatial memory), which is one of the main behavior tests to evaluate the mice model of Aβ1‐42‐induced dementia. [ABSTRACT FROM AUTHOR]

Aging is a normal physiological process accompanied by cognitive decline. This aging process has been the primary risk factor for development of aging-related diseases such as Alzheimer's disease (AD). Cognitive deficit is related to alterations of neurotrophic factors level such as brain-derived neurotrophic factor (BDNF), nerve growth factor (NGF) and glial cellderived neurotrophic factor (GDNF). These strong relationship between aging and AD is important to investigate the time which they overlap, as well as, the pathophysiological mechanism in each event. Considering that aging and AD are related to cognitive impairment, here we discuss the involving these neurotrophic factors in the aging process and AD. [ABSTRACT FROM AUTHOR]

Background: Foods rich in flavonoids are associated with a reduced risk of various chronic diseases, including Alzheimer's disease (AD). In fact, growing evidence suggests that consuming flavonoid- rich foods can beneficially affect normal cognitive function. Animal models have shown that many flavonoids prevent the development of AD-like pathology and improve cognitive deficits., Objective: Identifying the molecular causes underlying the memory-enhancing effect of flavonoid-rich foods makes it possible to provide the best diet to prevent cognitive decline associated with aging and Alzheimer's disease. Based on the most recent scientific literature, this review article critically examines the therapeutic role of dietary flavonoids in ameliorating and preventing the progression of AD and enhancement of memory with a focus on the role of the BDNF signaling pathway., Methods: The databases of PubMed, Web of Science, Google Scholar, and Scopus were searched up to March 2023 and limited to English language. Search strategies were using the following keywords in titles and abstracts: (Flavonoid-rich foods OR Flavonoids OR Polyphenols); AND (Brain-Derived Neurotrophic Factor OR BDNF OR CREB OR) AND (Alzheimer's disease OR memory OR cognition OR)., Results: Flavonoid-rich foods including green tea, berries, curcumin and pomegranate exert their beneficial effects on memory decline associated with aging and Alzheimer's disease mostly through the direct interaction with BDNF signaling pathway., Conclusion: The neuroprotective effects of flavonoid-rich foods through the CREB-BDNF mechanism have the potential to prevent or limit memory decline due to aging and Alzheimer's disease, so their consumption throughout life may prevent age-related cognitive impairment., (Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.)