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With the growth of the aging population, the prevalence of Alzheimer's disease (AD) has increased and influenced the work and daily life of AD patients, imposing a heavy burden on society and the patients' families. AD is a progressive disease with a long duration, and the pathogenesis is very complicated. Here, we found that alpha-lipoic acid (LA), an endogenous, naturally synthesized compound, could attenuate amyloid beta fragment (Aβ25-35 )-induced PC12 cell toxicity. Aβ25-35 treatment largely decreased the viability of PC12 cells, increased reactive oxygen species (ROS) levels, and increased the percentage of apoptotic cells, which were accompanied by changes in the expression of the apoptosis-related genes. Further, the Wnt pathway was inactivated, and the expression of Wnt pathway-related proteins such as Frizzled2, GSK3β, and phosphorylated GSK3β were dysregulated after Aβ25-35 treatment. LA efficiently attenuated Aβ25-35 -induced PC12 cell apoptosis and downregulated the phosphorylation-mediated degradation of β-catenin as well as GSK3β. Our results demonstrate that LA rescues Aβ25-35 -induced neurocytotoxicity through the Wnt-β-catenin pathway.

Lipoic acid (LA) is identified as an antioxidant to scavenge and inactivate free radicals. Although LA has been used as a dietary supplement for a long time, the effect of LA supplement on preventing aged-memory loss haven’t been studied yet. This study aimed to determine whether LA could promote the ability of learning and memory in the aged mice model. There were four groups in this study: aged control group (20 months old C57BL / 6J mice without any dosage), 0.1% LA dosage group (20 months old C57BL / 6J mice), 0.2% LA dosage group (20 months old C57BL / 6J mice), and young control group(3 months old C57BL / 6J mice without any dosage). Cognitive abilities were tested through behavioral tests, and factors related to synaptic plasticity (BDNF, PSD95, p-NMDAR1, p-CAMK II) were detected by Western Blot. In behavioral test, young control group shown a greater capacity in learning and memory than aged control group. Comparing with aged control group, the abilities of passive avoidance and spatial memory and learning in two LA dosage groups were significantly enhanced by using step-down test and Morris water maze respectively. Up-regulated expression of BDNF and higher levels of PSD95, p-NMDAR1, p-CAMKⅡ were observed in both two LA dosage groups and young control group compared with aged control group. Our findings suggest that long-term LA intervention can effectively delay or prevent the decline of learning and memory associated with aging via altered synaptic plasticity.

In June 2020, the new “Regulations on the Supervision and Administration of Cosmetics” (CSAR) was finally issued and published in China. This is the first revision of the “Regulations on Hygiene Supervision of Cosmetics” (CHSR) since its publication in 1989. As the basic and fundamental legislation for cosmetics, CSAR has a far-reaching impact on the whole industry and also reveals new trends in scientific research work. To provide an interpretation of this regulation and help enterprises and researchers better understand the new policies, in this study, the main contents of CSAR and its regulatory system were introduced, and the major changes and background considerations were summarized, especially in the definition and scope of cosmetics, classification and categorization, ingredient management, safety evaluation, efficacy substantiation and technical evaluation work. A brief review of technical progress worldwide and a comparison of regulatory requirements were provided where necessary. Finally, new prospects of cosmetic science in China were discussed. In conclusion, CSAR will initiate a renewed and integrated regulatory system for cosmetics. Advanced concepts of supervision, encouragement of innovation, utilization of technical approaches and emphasis on scientific investigations are reflected in the regulations, which will deeply influence the development of both cosmetic products and new ingredients. With all these new challenges and opportunities, everyone involved should get prepared.

BACKGROUND: A marine oligopeptide preparation (MOP) obtained from Chum Salmon (Oncorhynchus keta) by the method of enzymatic hydrolysis, has been found to enhance the innate and adaptive immunities through stimulation of the secretion of cytokines in mice. The current study aimed to further investigate the protective effect of MOP on radiation-induced immune suppression in mice. RESULTS: Female ICR mice (6–8 weeks old) were randomly divided into three groups, i.e. blank control, irradiation control and MOP (1.350 g kg−1 body weight) plus irradiation-treated group. MOP significantly increased the survival rate and prolonged the survival times for 30 days after irradiation, and lessened the radiation-induced suppression of T- or B-lymphocyte proliferation, resulting in the recovery of cell-mediated and humoral immune functions. This effect may be produced by augmentation of the relative numbers of radioresistant CD4+ T cells, enhancement of the level of immunostimulatory cytokine, IL-12, reduction of the level of total cellular NF-κB through the induction of IκB in spleen and inhibition of the apoptosis of splenocytes. CONCLUSION: We propose that MOP be used as an ideal adjuvant therapy to alleviate radiation-induced injuries in cancer patients. Copyright © 2010 Society of Chemical Industry

To observe the neuroprotective effects of marine collagen peptide (MCP) isolated from Chum Salmon (Oncorhynchus keta) skin by enzymatic hydrolysis, 20-month-old female C57BL/6J mice were fed with chow diet, 0.22%, 0.44% or 1.32% (wt/wt) MCP diet for 3 months. Comparing with aged control group, the abilities of passive avoidance and spatial memory and learning were significantly enhanced evaluated by step-down test and Morris water maze respectively. Furthermore, the abilities of learning and memory had no significant difference between 0.44% and 1.32% MCP treated groups and young control group. The alleviated oxidative stress, reduced apoptotic neurons, up-regulated expression of brain-derived neurotrophic factor (BDNF) and postsynaptic density protein 95 (PSD95) were observed in MCP treated groups compared with aged control group. Our research revealed that there were no significant difference between 0.44% and 1.32% MCP treated groups and young control group. These findings suggest that MCP could be a candidate for functional food to relieve memory deficits associated with aging.

Flavonoid-rich foods have been shown to be effective at reversing age-related deficits in learning and memory in both animals and humans. However, little investigation of the preventative effects of flavonoids on the naturally aged animals was reported. In our study, 14-month-old female C57BL/6 J mice were orally administered 0.025%, 0.05% and 0.1% green tea catechins (GTC, w/v) in drinking water for 6 months; we found that a supplementation with 0.05% or 0.1% GTC prevented age-related spatial learning and memory decline of mice in the Morris water maze. Better performance of GTC-treated mice was associated with increased levels of cAMP-response element binding protein (CREB) phosphorylation in the hippocampus. The expressions of brain-derived neurotrophic factor (BDNF) and Bcl-2, two target genes of CREB which can exhibit long-term regulatory roles in synaptic plasticity and synaptic structure, were also increased. We also found that long-term 0.05% or 0.1% GTC administration prevented age-related reductions of two representative post-synaptic density proteins PSD95 and Ca(2+)/calmodulin-dependent protein kinase II, suggesting that synaptic structural changes may be involved. These results demonstrated that long-term 0.05% or 0.1% green tea catechin administration may prevent age-related spatial learning and memory decline of female C57BL/6 J mice by regulating hippocampal CREB signaling cascade.

To observe the immunomodulatory effects of marine oligopeptide preparation (MOP) from Chum Salmon ( Oncorhynchus keta ) by the method of enzymatic hydrolysis, female ICR mice (6–8 weeks old) were administered the MOP for four weeks with the dose of 0, 0.22, 0.45 and 1.35 g/kg/body weight. In comparison with the control group, the MOP could significantly enhance the capacity of lymphocyte proliferation induced by the mitogen concanavalin A, the number of plaque-forming cells, natural killer cell activity, the percentage of CD4 + T helper (Th) cells in spleen and the secretion of Th1 (IL-2, IFN-γ) and Th2 (IL-5, IL-6) type cell cytokines. Nevertheless, no significant differences in weight gain, lymphoid organ indices and phagocytosis capacity were observed in our study. These results suggest that MOP is a possible immune stimulant and may strengthen the immune response of its host.

Ginsenoside, the effective component of ginseng, has been reported to have a neuron protective effect, but the preventive effect on Alzheimer's disease (AD) related memory loss and the underlying mechanisms have not been well determined. The senescence-accelerated mouse (SAM) is a useful model of AD-related memory impairment. In the present study, SAMP8 mice aged 4 months were chronically treated with ginsenoside (3 dose groups were given ginsenoside in drinking water for 7 months). The three groups were treated with ginsenoside 50, 100 and 200 mg/kg per day, respectively. Placebo-treated aged mice and young ones (4 months old) were used as controls. In addition, SAMR1 mice were used as "normal aging" control. The beneficial role of ginsenoside was manifested in the prevention of memory loss in aged SAMP8 mice. The optimal dose of ginsenoside is 100 or 200 mg/kg per day. In ginsenoside treated groups, the Abeta level markedly decreased in hippocampus and antioxidase level significantly increased in serum. In addition, the plasticity-related proteins in hippocampus significantly increased in the two ginsenoside treated groups. The plasticity-related proteins were checked in the present study including postsynaptic density-95 (PSD-95), phosphor-N-methyl-D-aspartate receptor 1 (p-NMDAR1), phospho-calcium-calmodulin dependent kinase II (p-CaMKII), phospho-protein kinase A Catalyticbeta subunit (p-PKA Cbeta) and protein kinase Cgamma subunit (PKCgamma), phospho-CREB (p-CREB) and brain derived neurotrophic factor (BDNF) etc. These findings suggest that the increase of antioxidation and up-regulation of plasticity-related proteins in hippocampus may be one of the mechanisms of ginsenoside on the memory loss prevention in aged SAMP8 mice.

microRNAs (miRNAs) play an important role in development and are associated with birth defects. Data are scant on the role of miRNAs in birth defects arising from exposure to environmental factors such as alcohol.In this study, we determined the expression levels of 509 mature miRNAs in fetal mouse brains with or without prenatal ethanol exposure using a miRNA microarray technique, verified by northern blot and PCR. Mouse embryos in culture were used to examine the effect of ethanol treatment on expression of the putative target genes of miR-10a (Hoxa1 and other Hox members) at mRNA and protein level. Open field and Morris water maze tests were also performed at post-natal day 35.Ethanol treatment induced major fetal teratogenesis in mice and caused mental retardation in their offspring, namely lower locomotor activity (P0.01) and impaired task acquisition. Of the screened miRNAs, miR-10a, miR-10b, miR-9, miR-145, miR-30a-3p and miR-152 were up-regulated (fold change1.5) in fetal brains with prenatal ethanol exposure, whereas miR-200a, miR-496, miR-296, miR-30e-5p, miR-362, miR-339, miR-29c and miR-154 were down-regulated (fold change0.67). Both miR-10a and miR-10b were significantly up-regulated (P0.01) in brain after prenatal ethanol exposure. Ethanol treatment also caused major obstruction in the development of cultured embryos, with down-regulated Hoxa1. Co-incubation with folic acid blocked ethanol-induced teratogenesis, with up-regulated Hoxa1 and down-regulated miR-10a (P0.01).The study provided new insights into the role of miRNAs and their target genes in the pathogenesis of fetal alcohol syndrome.

Due to the increased consumption of marine collagen peptides preparation (MCP) as ingredients in functional foods and pharmaceuticals, it was necessary to carry out safety requirements in the form of an oral chronic toxicity assessment. In order to define the oral chronic toxicity of MCP, a 24-month feeding study of MCP was carried out. Sprague-Dawley (S-D) rats at the age of four-week of both sexes were treated with MCP at the diet concentrations of 0%, 2.25%, 4.5%, 9% and 18% (wt/wt). The actual food intake and bodyweight of the individual animals were recorded periodically until sacrifice. Blood and urine samples were collected for serum chemistry evaluations and urinalysis. Throughout the experimental period, there was no toxicologically significant difference between the vehicle and MCP-treated animals with respect to the survival rate, body weight, food consumption, urinalysis, clinical biochemistry parameter and relative organ weight in either sex. Moreover, incidences of non-neoplastic lesions in MCP-treated groups did not significantly increase compared with the control group. Under the present experimental conditions, no higher risk of chronic toxic effects was observed in MCP-treated rats at the diet concentrations of 2.25%, 4.5%, 9% and 18% (wt/wt) than in the rats fed with basal rodent diet.

Marine oligopeptide preparation (MOP) obtained from Chum Salmon (Oncorhynchus keta) by the method of enzymatic hydrolysis, has been found to possess a radioprotective property through stimulation of the radiation-induced immunosuppression. The current study aimed to further investigate the free radicals scavenging and antioxidant effects of MOP in radiation injured mice. Female ICR mice (6–8 weeks old) were randomly divided into 5 groups, i.e., blank control, irradiation control and MOP (0.225, 0.450 and 1.350 g/kg body weight) plus an irradiation-treated group. The result revealed that MOP significantly increased the white blood cell counts after irradiation, and lessened the radiation-induced oxidative damage. These effects may be caused by augmentation of the activities of antioxidant enzymes, such as SOD and GSH-Px, reduction of the lipid peroxidation (MDA level) in liver, and protection against radiation-induced apoptosis. Therefore, we propose that MOP be used as an ideal antioxidant to alleviate radiation-induced oxidation damage in cancer patients.

A marine oligopeptide preparation (MOP) obtained from Chum Salmon (Oncorhynchus keta) by the method of enzymatic hydrolysis, has been found to enhance the innate and adaptive immunities through stimulation of the secretion of cytokines in mice. The current study aimed to further investigate the protective effect of MOP on radiation-induced immune suppression in mice.Female ICR mice (6-8 weeks old) were randomly divided into three groups, i.e. blank control, irradiation control and MOP (1.350 g kg(-1) body weight) plus irradiation-treated group. MOP significantly increased the survival rate and prolonged the survival times for 30 days after irradiation, and lessened the radiation-induced suppression of T- or B-lymphocyte proliferation, resulting in the recovery of cell-mediated and humoral immune functions. This effect may be produced by augmentation of the relative numbers of radioresistant CD(4) (+) T cells, enhancement of the level of immunostimulatory cytokine, IL-12, reduction of the level of total cellular NF-κB through the induction of IκB in spleen and inhibition of the apoptosis of splenocytes.We propose that MOP be used as an ideal adjuvant therapy to alleviate radiation-induced injuries in cancer patients.

To observe the effects of marine collagen peptides (MCPs) on blood glucose and lipid metabolism in hyperinsulinemic rats.Male SD rats fed with high fat diet for 4 months were used to establish a hyperinsulinemic model. Thirty two hyperinsulinemic rats were divided into four groups according to body weight and serum insulin level, namely hyperinsulinemic control (HIC) group and 3 Marine Collagen Peptides treated groups with 8 rats in each group. Another 8 healthy male SD rats fed with basic diet were used as negative control (NC). Rats in MCPs groups were treated by intragastric way with MCPs at the dose of 0.225 g/kg bw, 0.45 g/kg bw and 1.35 g/kg bw respectively for 8 weeks, while rats in HIC and NC groups were treated with tap water in the same manner. During the test period, rats in HIC and MCPs groups were fed with high fat diet sequentially, while rats in NC group were fed with basic diet. Fasting serum glucose (GLU), insulin (INS) and lipids were assayed respectively before and after MCPs treatment. Oral glucose tolerance test, antioxidase activity, serum malondialdehyde (MDA) levels and the ultrastructure of islet beta cell were carried out at the end of the experiment.After 8 weeks of treatment, compared with HIC group, fasting INS, TC and TG of all three MCPs-treated groups decreased obviously, while fasting GLU level lowered significantly in 0.225 g/kg bw and 1.35 g/kg bw MCPs groups. Moreover, GLU level at 0.5 h, 2 h and the area under blood sugar curve in OGTT were evidently lower in 0.45 g/kg bw and 1.35 g/kg bw MCPs groups. Besides, serum SOD activity increased in all MCPs groups, and serum GSH-Px activity elevated obviously in 1.35 g/kg bw MCPs group, while serum MDA reduced. Finally, the ultrastructural impairment of islet resulted from high fat diet was improved evidently by 1.35 g/kg bw MCPs.MCPs was effective in improving glucose and lipid metabolism in hyperinsulinemic rats induced by high fat diet.

The senescence-accelerated mouse prone-8 (SAMP8) is characterized by early onset of learning and memory deficits along with spontaneous overproduction of soluble beta-amyloid peptide (Abeta) in the brain. In our study, 4 month old male SAMP8 mice were orally administered 0.05% and 0.1% green tea catechins (GTC, w/v) in drinking water for 6 months. We found that a supplementation with 0.05% or 0.1% GTC prevented spatial learning and memory impairments of mice in the Morris water maze. Better performance of GTC-treated mice was associated with decreased levels of Abeta(1-42) oligomers in the hippocampus. The activity of the protein kinase A/cAMP-response element binding protein (PKA/CREB) pathway, one of the molecular targets of Abeta oligomers which is crucial for late long-term potentiation and long-term memory formation, was significantly increased after GTC administration. We also found that chronic 0.05% or 0.1% GTC consumption prevented the reductions of three representative proteins of synaptic function and synaptic structure, including brain-derived neurotrophic factor(BDNF), post-synaptic density protein-95 (PSD95) and Ca(2+)/calmodulin-dependent protein kinase II (CaMKII). These results demonstrated that long-term 0.05% or 0.1% green tea catechin administration may prevent spatial learning and memory decline of SAMP8 mice by decreasing Abeta(1-42) oligomers and upregulating synaptic plasticity-related proteins in the hippocampus.

article i nfo Several animal studies have showed that gelatin may be effective for minimizing bone loss in OVX rats with established osteopenia. To gain insight into how cod bone gelatin administration affects bone loss after ovariectomy, studies were carried out focusing on bone quality and the molecular mechanisms. Eighty-four female rats were ovariectomized,12 sham-operated, divided into six groups of 12 each and treated one week after ovariectomy either with vehicle or cod bone gelatin (0.375, 0.75, 1.5, 3, 6 mg/kg body weight) for 90 days. Bone densitometry, μCT analysis, real-time PCR analysis and biochemical analysis were used at the end of the study. After 90 days, BMD of proximal tibia and femoral neck decreased in OVX rats, whereas the loss of BMD in those regions was prevented at 3 g/kg (Pb0.05). However, the BMD of midshaft femurs showed no significant differences. BV/TV, Tb.N. and Tb.Th. in the 3 g/kg group were, respectively, 30.4% (Pb0.05), 145.5% (Pb0.05) and 81.5% (Pb0.05) higher than in the OVX group. A significant decrease was detected in urine CTX, NTX and DPD, suggesting decreased bone resorption. Treatment with 3 g/kg and 6 g/ kg cod bone gelatin attenuated the increase in serum IL-1β, IL-6 and TNF-α observed in the OVX group. Real- time PCR showed significantly decreased levels of mRNA expression for RANKL at the dosage of 6 g/kg and the RANKL/OPG mRNA ratio in the 3 g/kg and 6 g/kg group significantly decreased compared to the OVX group (Pb0.05). In conclusion, our data confirmed that the cod bone gelatin treatment at 3 g/kg is effective in the prevention of estrogen deficient bone loss by modulating the expression of RANKL and OPG and suppressing the release of proinflammatory cytokines.

Whole-embryo culture was used as the model system to study the effects of Di(2-ethylhexyl) phthalate (DEHP) on mice embryonic development. Mouse embryos (8.5 days old) during the period of organogenesis were exposed to immediately centrifugal serum (ICS) with DEHP at concentrations of: 0, 12.5, 25, 50, 100, 200 mg/L for 48 hours. The results showed that DEHP could cause damage to embryonic development and there was a significant dose-response and dose-effect relationship between concentration of DEHP and its embryonic developmental toxicity. At higher levels ((25 mg/L), DEHP could induce embryonic developmental retardation and significant morphological abnormalities. Abnormal heart, neural system, arch and small limb-bud development were the most common gross morphological abnormalities. But there was no significant increase in the number of nonviable embryos. The finding suggested that DEHP can induce developmental toxicity in vitro at higher level and teratogenicity may be the major effect.

In order to evaluate the developmental toxicity of BPA and to investigate the possible mechanism of it in vitro, whole embryo culture was used for the study. The embryos that removed from mother mice on gestational 8.5d (GD8.5) and mother rats on gestational 9.5d (GD9.5) were cultured immediately in centrifugal serum (ICS) with a series of concentrations of 0, 40, 60, 80, 100 mg/L of BPA for 48 h to evaluate the embryo development and morphological differentiation. The results showed that the BPA inhibited the development of embryos in vitro and there was a dose-response relationship between concentrations of BPA. At high level (or = 60 mg/L), BPA could delayed the growth and cardiac tube differentiation of visceral yolk sac (VYS), and induced various embryo defects, including abnormal neural system, arch, optic, flexion and small limb bud, etc. It is concluded that at high level, BPA had toxicity to mice and rat embryos in vitro. The damage on structure and function of VYS might be part of teratogenic mechanisms of BPA.

The micromass culture of Wistar rat embryo limb bud cells was used to investigate the characteristic of developmental toxicity of Bisphenol A (BPA) and its mechanism in vitro. The results showed that BPA inhibited both proliferation and differentiation of rat limb bud cells in vitro. The high level of BPA appeared to be cytotoxic to Wistar rat embryo limb bud cells in culture and inhibited the clone formation with dose-response relationship. The concentration of BPA for IP50 and ID50 were 38.74 mg/L and 27.93 mg/L respectively. According to Renaults' teratogenic criteria, BPA belonged to a positive teratogen. And the data suggested that the specific inhibition of cell proliferation and differentiation might be one of the mechanisms of high level BPA.