[Research on EGCG improving the degenerative changes of the brain in AD model mice induced with chemical drugs].

OBJECTIVE: To study the effect and mechanism of (-)-Epigallocatechin-3-gallate (EGCG) on the degeneretive changes of the brain in Alzheimer's disease (AD) model mice induced with chemical drugs. METHODS: AD model mice were established by subcutaneously injecting with 3% D-gal at the dose of 150 mg/kg body weight once daily for 6 weeks. From the third week, the mice of D-gal + V(E) 280 U/kg group, D-gal + EGCG 2 mg/(kg x d) group and D-gal + EGCG 6 mg/(kg x d) group were intragastricly given with 5.6% V(E) at the dose of 280 IU/kg and EGCG at the dose of 2 mg/kg x d or 6 mg/kg x d respectively after injection of D-gal. The mice of control group, D-gal + dd H2O group and D-gal + oil group were administered with same volume vehicle distilled water and soybean oil respectively. The pathological changes of the brain in AD model mice were observed by HE staining analysis, the immunohistochemical analysis of beta-amyloid (Abeta) and evaluating the expression of amyloid precursor protein (APP) in the hippocampus of mice by Western blot analysis. RESULTS: EGCG 2 mg/(kg x d) or 6 mg/(kg x d) 4 weeks, ig evidently released neuronal injury in the hippocampus of the AD mice induced by D-gal, and significantly reduced the express of Abeta and APP in the hippocampus of AD model mice induced by D-gal (P < 0.01). CONCLUSION: EGCG has a protective effect on AD model mice induced by D-gal by decreasing the expression of APP and beta-Amyloid in the hippocampus of mice.

[The expression changes of N-methyl-D-aspartic acid receptor in hippocampus of offspring from female rats exposed to aluminum in the pregnancy and lactation].

OBJECTIVE: To investigate the effects of aluminum on learning and memory and the expression of N-methyl-D-aspartic acid receptor (NMDAR) of hippocampus in offspring from female rats exposed to Al in the pregnancy or lactation, and to explore the mechanism of toxic effects of Al on central nervous system (CNS) during development. METHODS: The pregnant Wistar rats were randomly divided into 3 groups based on their body weight, i.e. control group was exposed to distilled water, low exposure group (0.2%AlCl3) and high exposure group (0.4%AlCl3) were exposed orally to AlCl3 in pregnancy and lactation for 6 weeks, 10 rats each group. Aluminum content in blood and brains was determined by atomic absorption spectrophotometry (AAS). Platform experiment was used to detect the abilities of learning and memory. The expression levels of NMDARs were detected by western blot assay. RESULTS: The Al content in blood and brains of rats in exposure groups increased significantly with Al dose, as compared with the control group (P < 0.05). In platform experiment, the incubation periods of rats in low and high exposure groups were (202.71 ± 81.99) and (19.67 ± 8.44) s respectively, which were significantly lower than that [(300.00 ± 0.00) s] in control group (P < 0.01), but the mistake times of rats in low and high exposure groups were 1.43 ± 0.85 and 2.47 ± 0.99 respectively, which were significantly higher than that (0.00 ± 0.00) in control group (P < 0.01). The Al exposure could change the proportion of NMDAR subtypes, the expression levels of NR1 and NR2B in hippocampus of newborn rats in low and high exposure groups were 25.22 ± 0.68, 81.23 ± 15.37 and 24.75 ± 0.71, 56.63 ± 7.82, respectively, which were significantly lower than those (31.69 ± 3.44, 107.61 ± 9.05) in control group (P < 0.05). CONCLUSION: Aluminum exposure in pregnancy and lactation could reduce the abilities of learning and memory in newborn rats, and change the proportion of NMDAR subtypes. The reduced NR1 and NR2B expression levels may be one of important mechanisms to influence the abilities of learning and memory in offspring.