中文摘要：

目的分析川芎嗪预处理大鼠肾上腺嗜铬细胞瘤细胞株PC12细胞后过氧化氢诱导的细胞凋亡情况,探讨川芎嗪抑制脑缺血损伤中氧自由基损伤的分子机制。方法采用川芎嗪预处理PC12细胞后,制备过氧化氢细胞损伤模型,采用CCK-8法活细胞检测、Hoechst-33342染色、流式细胞术、反转录聚合酶链反应分析细胞凋亡发生机制。结果应用0.0、0.1、1.0、10.0 mmol/L浓度川芎嗪预处理后,细胞活力分别为（51.2±4.64）%、（58.5±7.46）%、（73.8±2.94）%、（81.0±6.06）%（F=146.9,P〈0.05）,细胞未见大量凋亡小体形成,Bax/Bcl-2比值降低（F=2.14,P〈0.05）,线粒体膜电位提高,Caspase 3、9活性降低（Caspase 3：F=1.59,P〈0.05;Caspase9：F=4.98,P〈0.05）。结论川芎嗪预处理后可降低过氧化氢诱导的PC12细胞凋亡,抑制氧自由基损伤。

英文摘要：

Objective To analyze the protection of tetramethylpyrazine to PC12 cells from apoptosis induced by H2O2 and to explore the inhibition mechanisms of oxygen free radical injury in cerebral ischemia.Methods After the PC12 cells were pretreated by tetramethylpyrazine,H2O2 was added to induce the apoptosis of PC12 cells.Various methods,including CCK-8live cell test,Hoechst-33342 staining,flow cytometry and quantitative reverse transcription polymerase chain reaction（qRT-PCR）,were used to analyze the mechanisms involved in the process.Results After the different concentrations（0,0.1,1,10mmol/L）tetramethylpyrazine pretreatment,there were no large number of apoptotic bodies formed in PC12 cells and the viability（%）of PC12 cells were（51.2±4.64）%,（58.5±7.46）%,（73.8±2.94）% and（81.0±6.06）% respectively（F=146.9,P〈0.05）.Moreover,in PC12 cells,the rate of Bax/Bcl-2dropped（F=2.14,P〈0.05）,the electric potential of mitochondrial membrane enchanced,activity of Caspase 3and Caspase 9decreased（Caspase 3：F=1.59,P〈0.05;Casapse 9：F=4.98,P〈0.05）.Conclusion The pretreatment with tetramethylpyrazine could reduce the apoptosis of PC12 cells damaged by H2O2 and inhibit oxygen free radical injury.