论文部分内容阅读
目的:研究(-)表没食子儿茶素没食子酸酯(epigallocatechin-3-gallate,EGCG)对阿尔茨海默病(AD)模型小鼠的脑部退行性病变的作用及作用机制。方法:给小鼠每日按150 mg/kg皮下注射3%的D-半乳糖(D-galac-tose,D-gal),连续注射42 d,以制备AD小鼠脑部退行性病变模型;造模14 d后每日给EGCG低、高剂量组小鼠按2mg/kg灌胃0.04%或0.12%的EGCG 1次,VE阳性对照组小鼠按280 U/kg灌胃5.6%VE1次,连续给药28 d。通过对各组小鼠脑部HE染色、海马区β-淀粉样肽(Aβ)免疫组化分析及Western blot检测β-淀粉样肽前体蛋白(APP)的蛋白表达水平,观察EGCG对AD模型小鼠脑部病理改变的影响及作用机制。结果:EGCG显著减轻了D-半乳糖诱导的AD模型小鼠海马神经元的损伤,并显著减少了D-半乳糖诱导AD小鼠海马区的Aβ及APP蛋白表达水平(P<0.01)。结论 EGCG可能通过降低D-半乳糖诱导的APP含量的增加及Aβ的毒性作用,发挥对D-半乳糖诱导的AD模型鼠的脑部病理改变的保护作用。
AIM: To investigate the effect of (-) epigallocatechin-3-gallate (EGCG) on degenerative brain diseases in mice with Alzheimer’s disease (AD) and its possible mechanism. Methods: The mice were injected subcutaneously with D-galactose (D-galactose) at a dose of 150 mg / kg for 42 days to prepare a model of degenerative brain disease in AD mice. The mice in EGCG low and high dose groups were intragastrically given 0.04% or 0.12% EGCG once daily for 2 mg / kg after 14 d of modeling. The mice in VE positive control group were intragastrically infused by 280 U / kg for 5.6% VE 1 times, Continuous dosing 28 d. The protein expression of β-amyloid precursor protein (APP) was detected by HE staining, immunohistochemical analysis of β-amyloid peptide (Aβ) in hippocampus and Western blot, and the effect of EGCG on AD model Effect of brain pathological changes in mice and its mechanism. Results: EGCG significantly reduced the damage of hippocampal neurons induced by D-galactose in AD model mice and significantly decreased the expression of Aβ and APP in hippocampus of AD mice induced by D-galactose (P <0.01). Conclusion EGCG may play a protective role in the pathological changes of brain in AD model mice induced by D-galactose by decreasing the increase of APP content induced by D-galactose and the toxic effect of Aβ.