β-淀粉样蛋白通过激活caspase-3诱导PC12细胞凋亡

β-AMYLOID INDUCES APOPTOSIS OF PC12 CELLS THROUGH ACTIVATING CASPASE-3

目的探讨β-淀粉样蛋白25-35片段(Aβ25-35)对体外培养的大鼠嗜铬瘤细胞PC12细胞促凋亡机制。方法采用四甲基偶氮唑蓝(MTT)法观察不同浓度的Aβ25-35干预PC12细胞24h后的细胞活性;将细胞分为对照组、实验组(即20 mmol/L Aβ25-35组),流式细胞技术观察两组PC12细胞凋亡率;免疫细胞化学染色法观察PC12细胞凋亡基因caspase-3的表达。结果PC12细胞活性呈Aβ25-35剂量依赖性降低,且浓度为20 mmol/L时降低最显著;PC12细胞实验组的凋亡率为23.03%±1.22%,对照组为2.42%±0.87%(P<0.01);caspase-3实验组的阳性表达较对照组明显增加(P<0.01)。结论Aβ可通过激活促凋亡基因caspase-3诱导PC12细胞凋亡。

Objective To study the mechanism of apoptosis induced by amyloid beta-peptide fragment 25-35（Aβ25-35）in PC12 cells.MethodsMTT assay was used to measure the viability of PC12 cells treated by different concentrations of Aβ25-35 for 24 hours;The cells were divided into the control group and the experimental group（20mmol/L Aβ25-35 group）,The apoptotic proportion was detected by flow cytometry,and the positive expression of caspase-3 was observed by immunocytochemistry.ResultsAfter exposure of PC12 cells to different concentrations of Aβ25-35,accompanied with decreased cell viability,especially in the concentration of 20mmol/L,the proportion of apoptotic cells in the experimental group was 23.03%±1.22%,but in control group it was 2.42%±0.87%（P〈0.01）.The positive expression of caspase-3 in the experimental group was higher than that of the control group（P〈0.01）.ConclusionAβ25-35 can induce PC12 cell apoptosis by promoting caspase-3 expression.