CAJ | 학술논문

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 V-FITC/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。
목적：탐토소벽감대Aβ25～35손상신경원적보호궤제。방법채용25μmol/LAβ25～35작용우원대배양대서해마신경원36 h，복제아이자해묵병（AD）세포모형，예선혹동시가입1、2、4μmol/L소벽감진행간예。채용세포증식억제시험（MTT）법평개세포존활솔，통과 Annexin V-FITC/PI쌍표류식세포술검측조기조망정황，Western인적검측활화적 Caspase-3단백표체。결과여대조조비교，AD세포모형신경원세포존활솔명현하강，조망명현증가（P＜0.01）。소벽감능구제고모형조세포적생존솔，4μmol/L소벽감능현저감소 Aβ25～35손상신경원조기조망（P＜0.01），1、2μmol/L화4μmol/L소벽감분별사모형조세포활화적Caspase-3표체강저료30.4％、41.2％화63.1％。결론소벽감대AD세포모형구유일정신경보호작용，기작용궤제가능위억제Aβ25～35유도적세포조망。
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 signifi-cantly decreased under 4 μmol/L berberin treatment (P<0.01).The expression of activated caspase-3 protein in model group was respec-tively decreased by 30.4%, 41.2%and 63.1%under berberin treatment(1,2 and 4μmol/L).Conclusions Berberin exhibits the protec-tive effects against the cellular model of AD, its mechanism relates with the inhibition of cell apoptosis induced by Aβ25~35.