川芎嗪抑制肝癌HepG2细胞增殖及对线粒体凋亡途径的影响

通过研究川芎嗪(TMP)诱导肝癌HepG2细胞凋亡，探讨TMP抑制肝癌细胞增殖的作用机制。采用CCK-8法检测TMP对肝癌HepG2细胞增殖的影响及量效关系，进一步应用高内涵细胞成像分析系统(HCS)检测TMP对HepG2诱导细胞凋亡作用以及对细胞色素C的释放和线粒体跨膜电位的影响，并结合Western blot检测TMP对肝癌HepG2细胞cleaved-caspase-3和cleaved-caspase-9表达的影响。结果显示，TMP对HepG2细胞增殖有抑制作用，并呈现剂量依赖性，可显著诱导HepG2细胞凋亡，增加细胞色素C从线粒体中释放到细胞质中，且能降低HepG2细胞内线粒体跨膜电位水平，以及显著提高肝癌HepG2细胞中cleaved-caspase-3及cleaved-caspase-9的表达水平。结果表明，TMP具有抑制肝癌HepG2细胞增殖的作用，其作用机制可能与通过线粒体途径触发细胞凋亡有关。
The purpose of the present study was to investigate the anti-proliferative and apoptotic effects of tetramethypyrazine(TMP)on HepG2 and to elucidate the underlying mechanisms. CCK-8 was introduced to analyze the HepG2 cells proliferation. Cell apoptosis, mitochondrial membrane potential(ΔΨm)and cytochrome C were measured by high content screening(HCS). Cleaved-caspases protein expression was detected by Western blot. CCK-8 assay indicated that TMP significantly inhibited HepG2 cells proliferation in dose-dependent manner compared with the control group. Moreover, it was found that TMP could also induce HepG2 cell apoptosis, directly increase the release of cytochrome C, decrease ΔΨm and increase cleaved-caspase-3 and cleaved-caspase-9 protein expression. TMP may inhibit cell proliferation and induce cell apoptosis by stimulating the mitochondrial pathway apoptosis in HepG2 cells