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目的探讨胞浆内的Ca~(2+)在顺铂诱导的肝癌HepG2细胞凋亡过程中的作用及其可能机制。方法体外培养人肝癌HepG2细胞,分组并按实验目的加药,检测胞浆内Ca~(2+)浓度的变化和Grp78蛋白的表达;MTT法检测细胞的活力;流式细胞仪检测细胞凋亡率。结果顺铂诱导了肝癌HepG2细胞内胞浆Ca~(2+)表达增加,促进细胞凋亡,同时也上调了Grp78蛋白的表达。与顺铂组相比,顺铂联合BAPTA/AM或2-APB降低了顺铂诱导的胞浆Ca~(2+)浓度,减弱了顺铂对细胞的增殖抑制作用和Grp78蛋白的表达。结论顺铂诱导HepG2细胞发生内质网应激,导致Ca~(2+)从内质网释放,使胞浆内Ca~(2+)上调,并进一步诱导内质网应激介导的凋亡。
Objective To investigate the role of cytoplasmic Ca ~ (2+) in cisplatin-induced HepG2 cell apoptosis and its possible mechanism. Methods Human hepatocellular carcinoma HepG2 cells were cultured in vitro and divided into groups according to the purpose of experiment. The changes of Ca 2+ concentration and Grp78 protein in cytoplasm were detected by MTT assay. The apoptosis of HepG2 cells was detected by flow cytometry rate. Results Cisplatin induced an increase of Ca 2+ in cytoplasm of hepatocellular carcinoma HepG2 cells, promoted cell apoptosis and up-regulated the expression of Grp78 protein. Compared with the cisplatin group, cisplatin combined with BAPTA / AM or 2-APB decreased cisplatin-induced cytoplasmic Ca 2+ concentration and attenuated the inhibitory effect of cisplatin on cell proliferation and Grp78 protein expression. Conclusion Cisplatin induces endoplasmic reticulum stress in HepG2 cells, which leads to the release of Ca ~ (2+) from the endoplasmic reticulum, upregulation of intracellular Ca ~ (2+) and further induction of endoplasmic reticulum stress-mediated apoptosis Death.