摘要
目的探讨小檗碱对Aβ25~35损伤神经元的保护机制。方法采用25μmol/LAβ25~35作用于原代培养大鼠海马神经元36 h,复制阿尔茨海默病(AD)细胞模型,预先或同时加入1、2、4μmol/L小檗碱进行干预。采用细胞增殖抑制试验(MTT)法评价细胞存活率,通过Annexin VFITC/PI双标流式细胞术检测早期凋亡情况,Western印迹检测活化的Caspase-3蛋白表达。结果与对照组比较,AD细胞模型神经元细胞存活率明显下降,凋亡明显增加(P<0.01)。小檗碱能够提高模型组细胞的生存率,4μmol/L小檗碱能显著减少Aβ25~35损伤神经元早期凋亡(P<0.01),1、2μmol/L和4μmol/L小檗碱分别使模型组细胞活化的Caspase-3表达降低了30.4%、41.2%和63.1%。结论小檗碱对AD细胞模型具有一定神经保护作用,其作用机制可能为抑制Aβ25~35诱导的细胞凋亡。
Objective To investigate the protective mechanism of berberin on the hippocampus neurons of rat injured by Aβ25 ~ 35.Methods Aβ25 ~ 35 was used to treat the hippocampus neurons of primary culture rat,at the final concentration of 25 μmol /L for 36 hours,Alzheimer's disease(AD) model was reproduced,and then interfered with berberin(1,2 and 4 μmol /L). MTT assay was used to observe the cell vitality; Annexin V-FITC /PI double stain flow cytometry assay was used to examine the early neural apoptosis,Western blot was used to observe the expression of activated caspase-3 protein. Results The cell vitality in AD model was decreased and the early neural apoptosis of AD model was significantly increased compared with the control group(P < 0. 01). The early cell apoptosis induced by Aβ25 ~ 35 was significantly decreased under 4 μmol /L berberin treatment(P < 0. 01). The expression of activated caspase-3 protein in model group was respectively decreased by 30. 4%,41. 2% and 63. 1% under berberin treatment(1,2 and 4 μmol /L). Conclusions Berberin exhibits the protective effects against the cellular model of AD,its mechanism relates with the inhibition of cell apoptosis induced by Aβ25 ~ 35.
出处
《中国老年学杂志》
CAS
CSCD
北大核心
2014年第20期5794-5796,共3页
Chinese Journal of Gerontology
基金
国家自然科学基金(81301041)
陕西省教育厅基金(14JK1627)
