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目的观察骨形成蛋白-2(bone morphogenetic protein-2,BMP-2)对人肝癌HepG-2细胞凋亡的作用及其信号通路机制。方法用流式细胞分析和细胞凋亡ELISA法检测HepG2细胞凋亡,用Western blot法检测丝裂原激活蛋白激酶(MAPKs)和磷脂酰肌醇3-激酶(PI3K)下游效应因子Akt的激活,采用信号通路阻断剂预处理HepG2细胞观察BMP-2影响细胞凋亡的机制。结果BMP-2诱导HepG2细胞凋亡,呈时间和剂量依赖性;BMP-2激活HepG2细胞JNK激酶,但不能激活ERK1/2、p38及Akt;采用JNK信号通路抑制剂SP600125可阻断BMP-2对HepG-2细胞JNK的激活,并消除BMP-2对HepG-2细胞凋亡的作用。结论BMP-2通过JNK信号通路途径诱导HepG2肝癌细胞凋亡。
Objective To observe the effect of bone morphogenetic protein-2 (BMP-2) on the apoptosis of human hepatoma HepG-2 cells and its signaling pathway. Methods The apoptosis of HepG2 cells was detected by flow cytometry and apoptosis ELISA. The activation of Akt, a downstream effector of mitogen-activated protein kinases (MAPKs) and phosphatidylinositol 3-kinase (PI3K), was detected by Western blot. HepG2 cells were pretreated with signal pathway blocker to observe the mechanism of BMP-2 in apoptosis. Results BMP-2 induced apoptosis in HepG2 cells in a time and dose-dependent manner. BMP-2 activated JNK kinase in HepG2 cells but not ERK1 / 2, p38 and Akt. JNK signaling pathway inhibitor SP600125 blocked BMP-2 On HepG-2 cells JNK activation, and to eliminate BMP-2 on HepG-2 cell apoptosis. Conclusion BMP-2 induces apoptosis of HepG2 hepatocarcinoma cells through JNK signaling pathway.