[高氯酸钾血竭素诱导Hela细胞凋亡的机制]
[Mechanism of dracorhodin perchlorate-induced Hela cell apoptosis].
作者信息
Xia Ming-yu, Wang Min-wei, Wang Hao-ran, Tashiro Shin-ichi, Ikejima Takashi
机构信息
China-Japan Research Institute of Medical and Pharmaceutical Sciences, Shenyang Pharmaceutical University, Shenyang 110016, China.
出版信息
Yao Xue Xue Bao. 2004 Dec;39(12):966-70.
AIM
To study the mechanism of dracorhodin perchlorate-induced Hela cell apoptosis.
METHODS
Cell viability was measured by MTT method. Morphological changes were observed by phase contrast microscopy and Hoechst 33258 staining. DNA fragmentation was assayed by agarose gel electrophoresis. Protein expression was detected by Western blot analysis.
RESULTS
Dracorhodin perchlorate induced Hela cell apoptosis. The apoptosis was partially reversed by caspase-1, -3, -8, -9 and caspase family inhibitors. Treatment of Hela cells with dracorhodin perchlorate for 12 h increased the protein expression ratio of Bax/Bcl-XL; procaspase-3, -8, ICAD and PARP were cleaved to smaller molecules.
CONCLUSION
Dracorhodin perchlorate induced Hela cell death via alteration of Bax/Bcl-XL ratio and activation of caspases.
目的
研究高氯酸血竭素诱导人宫颈癌HeLa细胞凋亡的机制。
方法
采用MTT法检测细胞活力。通过相差显微镜和Hoechst 33258染色观察形态学变化。用琼脂糖凝胶电泳检测DNA片段化。通过蛋白质免疫印迹分析检测蛋白表达。
结果
高氯酸血竭素诱导HeLa细胞凋亡。半胱天冬酶-1、-3、-8、-9及半胱天冬酶家族抑制剂可部分逆转这种凋亡。用高氯酸血竭素处理HeLa细胞12小时后，Bax/Bcl-XL蛋白表达比率增加；前半胱天冬酶-3、-8、ICAD和PARP被切割成小分子。
结论
高氯酸血竭素通过改变Bax/Bcl-XL比率和激活半胱天冬酶诱导HeLa细胞死亡。
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