摘要
Abstract
Objective To investigate the protective effect of triptolide against amyloid β-peptide 25-35 (Aβ25-35) induced injury of PC12 cells. Methods MTT assay was conducted to determine the optimal working concentration of Aβ25-35 for inducing PC12 cell injury model, and the potential protective effect of different concentrations of triptolide (1×10-11, 1×10-10 and 1×10-9 mol/L) on the PC12 cells. PC12 cells were randomly divided into 3 groups: control group, Aβ25-35 treatment group, and Aβ25-35 and triptolide co-treatment group. After 24-h treatment, active caspase-3 expression was observed by cyto-immunofluorescence. Meanwhile, Bcl-2 and Bax mRNA expressions were measured by RT-PCR. Results The in vitro PC12 cell injury model of Alzheimer's disease could be established by Aβ25-35 at a concentration of 10 μmol/L with a survival rate of (58 ± 6)%. Triptolide (1 ×10-11, 1 ×10-10 and 1 ×10-9 mol/L) alone had no significant effect on cell viability. Following the Aβ25-35 exposure, cell viability was significantly decreased. Furthermore, active caspase-3 protein and Bax mRNA expressions obviously increased after Aβ25 -35 treatment, while Bcl-2 mRNA expression decreased remarkably (P < 0.05). Triptolide, however, could significantly increase cell viability in a dose-dependent manner when it was added together with Aβ25 -35. Moreover, triptolide could also significantly suppress the expressions of active caspase-3 protein, Bcl-2 and Bax mRNA induced by Aβ25-35 (P<0.05).Conclusions Triptolide may inhibit cell apoptosis through modulation of expressions of active caspase-3, Bax and Bcl-2 to protect PC12 cells from Aβ25-35-induced cytotoxicity.关键词
雷公藤甲素/阿尔茨海默病/β-淀粉样蛋白/细胞凋亡Key words
triptolide/Alzheimer's disease/amyloid β-peptide/cell apoptosis分类
医药卫生
