中文摘要：

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。

英文摘要：

Objective To study the effect of cytosolic Ca^2＋ on cisplatin-induced HepG2 cells apoptosis. Methods HepG2 cells were treated with cisplatin （4 μg/ml） with or without BAPTA/AM （3 p, mol/L） and 2-APB （75 μmo//L） for 24 h. The confocal microscopy was used to observe free Ca^2＋ levels in the cytos01 and expression levels of Grp78. MTT assay was used to detect cell viability. The flow cytometry was used to detect cell apoptosis. Results Cisplatin increased cytosolic Ca^2＋ levels, inhibited cell viability, induced cell apoptosis, as well as enhanced the expression of Grp78. Compared with cisplatin group, treatment with cisplatin combined with BAFFA/AM or 2-APB decreased cytosolic Ca^2 ＋levels and promoted cell proliferation, as well as decreased the expression levels of Grp78. Conchision Cisplatin induces ER stress and subsequently triggers Ca^2＋ release from ER, followed by the increase of cytosolic Ca^2 ＋ levels, which can enhance ER stress-associated apoptosis.