辛伐他汀通过线粒体途径诱导K562细胞凋亡

目的观察辛伐他汀诱导K562细胞凋亡不同时间的膜电位(Δψm),caspase-3、9和细胞色素C的改变,以推测其凋亡通路。方法采用浓度为20μmol.L-1的辛伐他汀处理K562细胞24、48、72 h,采用流式细胞技术检测细胞凋亡率和线粒体膜电位,分光光度法检测caspase-3、9蛋白活性,免疫组织化学法检测细胞色素C蛋白。结果浓度为20μmol.L-1辛伐他汀作用K562细胞24、48、72 h后,凋亡率分别为(6.1±0.35)%、(14.15±0.42)%(、30.70±0.65)%,随着凋亡率增加线粒体膜电位降低分别为(39.6±4.80)%,(24.4±2.45)%,(6.0±1.62)%;caspase-3、9蛋白活性与对照组相比上调,细胞浆内细胞色素C升高。结论辛伐他汀诱导K562细胞凋亡时线粒体膜电位下降,caspase-3、9活性增高和细胞色素C释放,推测辛伐他汀诱导K562细胞的凋亡可能经过线粒体凋亡途径。

Simvastatin induces apoptosis in K562 cells through mitochondrial pathway

Objective To observe the changes of mitochondrial membrane potential(MMP),caspase-3,9 activity and cytochrome C,and determine the apoptosis signaling pathway in simvastatin-treatment K562 cells.Methods K562 cells were exposed in the 20 μmol/L simvastatin for different times(24 h,48 h,72 h).Flow cytometry were performed to confirm cell apoptotic ratio and analyze mitochondrial membrane potential;Colorimetric method was used to detect the caspase-3,9 activity;The protein of cytochrome C was detected by immunohistochemical method.Results K562 cells could undergo apoptosis after the treatment of 20 μmol/L simvastatin for 24 h,48 h and 72 h,and the apoptotic ratio are(6.1±0.35)%,(14.15±0.42)%,(30.70±0.65)%,respectively.There was a significant increase between the control groups and the text groups treated 24h.Furthermore,the percentages of MMP were(39.6±4.80)%,(24.4±2.45)%,(6.0±1.62)% at 24 h,48 h and 72 h respectively.The caspase-3,9 activity was increased compared with the control groups.The expression of cytochrome C in the 20 μmol/L simvastatin-induced K562 cell was increased.Conclusions The collapse of MMP,the up-regulated of caspase-3,9 activity and the increased cytochrome C are emerged after K562 cells treated by 20 μmol/L simvastatin.The apoptosis of K562 cells induced by simvastatin might be related to the mitochondrial pathway of apoptosis.