摘要
目的分析川芎嗪预处理大鼠肾上腺嗜铬细胞瘤克隆化细胞株PC12细胞后二甲酰胺诱导的细胞凋亡情况,探讨川芎嗪治疗脑缺血再灌注损伤的机制。方法采用川芎嗪预处理PC12细胞后,制备二甲酰胺细胞损伤模型,通过CCK-8法活细胞检测、Hoechst-33342染色、流式细胞术和实时荧光定量聚合酶链反应(RT-PCR)分析细胞凋亡发生机制。结果川芎嗪预处理后,PC12细胞的存活数提高,细胞未见大量核固缩及凋亡小体形成,总体凋亡率降低,caspase 3、caspase 9活性降低,线粒体膜电位提高,Bax/Bc l-2比值降低。结论川芎嗪预处理后可以降低二甲酰胺诱导的PC12细胞凋亡。
Objective To analyze whether tetramethylpyrazine could protect PC12 cell from apoptosis induced by diamide in order to explore the mechanism of tetramethylpyrazine in the treatment of cerebral ischemia-reperfusion injury.Methods After PC12 cells were cultured by tetramethylpyrazine,diamide was added to induce the apoptosis of PC 12 cells.Various methods,including CCK-8 live cell test,Hoechst-33342 staining,flow cytometry,and quantitative reverse transcription/polymerase chain reaction（RT-PCR）,were used to analyze the mechanisms involved in the process.Results After the pre-treatment,tetramethylpyrazine reduced the apoptosis of PC12 cells.The number of PC12 cells increased compared with decreased apoptosis rate.Tetramethylpyrazine could improve the activity of caspase 3,caspase 9 and the electric potential of mitochondrial membrane and the rate of Bax/Bcl-2 droped in the response to tetramethylpyrazine.Conclusions The pre-treatment with tetramethylpyrazine could reduce the apoptosis of PC12 cells damaged by diamide.
出处
《检验医学》
CAS
北大核心
2009年第12期907-910,共4页
Laboratory Medicine
基金
江苏省普通高校研究生创新基金资助项目(CXOJB-222z)
