INF-γ通过下调ATGL蛋白水平诱导肝癌细胞HepG2凋亡 INF-Gamma Induces HepG2 Apoptosis via Down-Regulating the Level of ATGL Protein

Abstract

目的：研究INF-γ通过ATGL诱导肝癌细胞HepG2凋亡的作用及分子机制。方法：ELISA法检测血清中INF-γ水平；MTT法检测肝癌细胞HepG2活力；Caspase-3酶活性试剂盒检测Caspase-3酶活性；过表达ATGL，研究INF-γ通过ATGL诱导肝癌细胞HepG2凋亡作用。结果：肝癌病人血清中INF-γ水平明显降低(P < 0.001)；INF-γ通过ATGL诱导肝癌细胞HepG2凋亡、促进Caspase-3酶活性升高和下调Bcl-2/Bax比例。结论：肝癌病人血清INF-γ水平降低，其通过下调ATGL蛋白诱导肝癌细胞HepG2凋亡。 Objective: To investigate the role and molecular mechanism of INF-gamma induced apoptosis of hepatocellular carcinoma cells (HepG2). Methods: ELISA method was used to detect the level of INF-gamma in serum. MTT assay was used to detect HepG2 proliferation, Caspase-3 enzyme activity kit was used to detect Caspase-3 enzyme activity. Overexpression of ATGL to investigate the molecular mechanism of INF-gamma induced apoptosis of hepatocellular carcinoma cells. Results: The level of INF-gamma in serum of liver cancer patients was significantly reduced. INF-gamma induced apoptosis of HepG2 cells, promoted the activity of Caspase-3 enzyme and down-regulated the proportion of Bcl-2/Bax through ATGL. Conclusion: The level of serum INF-gamma in liver cancer patients decreased and caused the apoptosis of HepG2 cells by down-regulating ATGL level.