晚期糖基化终产物对人肝癌细胞HepG2增殖的影响

目的探讨糖尿病晚期糖基化终产物(AGEs)对肝癌细胞HepG2增殖的影响及其机制。方法体外培养人肝癌细胞HepG2,以终浓度分别为100、200和400μg/ml的AGEs处理细胞24h,并设正常对照组进行比较。运用细胞计数试剂盒8研究AGEs对HepG2增殖的影响,流式细胞术检测细胞周期的改变,Western blot检测肝癌细胞抗凋亡基因表达。结果 AGEs呈浓度依赖性显著促进HepG2细胞增殖(P<0.05)。与对照组比较,200μg/ml AGEs干预24h后可以减少HepG2细胞G1期百分率,同时增加S期百分率(P<0.05)。AGEs可致细胞抗凋亡基因B细胞淋巴瘤-白血病2(Bcl-2)相关蛋白表达增加。结论 AGEs能促进HepG2细胞的增殖,其机制可能与上调Bcl-2相关蛋白表达,加速细胞G1期向S期转换相关。

Effects of AGEs on the proliferation of human hepatocellular carcinoma HepG2 cells

Objective To investigate the effects of advanced glycation end products(AGEs) on the proliferation of HepG2 cells and underlying mechanism. Methods Human hepatocellular carcinoma HepG2 cells were cultured and exposed to AGEs in the concentrations of 100,200 and 400 μg/ml for 24 hours in vitro.A normal control group was established for comparison.The proliferation of the HepG2 cells was assessed by CCK-8 assay. The cell cycles were analyzed by flow cytometry.Western blot method was used to detect the expression of anti-apoptosis protein. Results AGEs significantly promoted the proliferation of HepG2 cells in a dose-dependent manner(P<0.05).Compared with normal control group,the proportion of HepG2 cells was remarkably decreased in the G1 stage and increased in the S stage by AGEs in the concentration of 200 μg/ml(P<0.05).The expression of anti-apoptosis gene Bcl-2 protein was increased. Conclusion AGEs can promote the proliferation of human hepatocellular carcinoma HepG2 cells,possibly by upregulating the expression of Bcl-2 protein and accelerating the cell cycle from the G1 to S stage.