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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。
Objective To investigate the effects of advanced glycation end products (AGEs) on the proliferation of HepG2 hepatocellular carcinoma cells and its mechanism. Methods HepG2 cells were cultured in vitro and treated with AGEs at final concentration of 100, 200 and 400 μg / ml for 24 h respectively. The normal control group was also compared. The effects of AGEs on the proliferation of HepG2 cells were studied by using cell counting kit 8, the changes of cell cycle were detected by flow cytometry, and the expressions of anti-apoptotic genes were detected by Western blot. Results AGEs significantly promoted the proliferation of HepG2 cells in a concentration-dependent manner (P <0.05). Compared with the control group, the intervention of 200μg / ml AGEs for 24 hours reduced the percentage of G1 phase of HepG2 cells and increased the percentage of S phase (P <0.05). AGEs induced an increase in the expression of Bcl-2, an inhibitor of cellular anti-apoptotic gene B-cell lymphoma. Conclusion AGEs can promote the proliferation of HepG2 cells. The mechanism may be related to the up-regulation of Bcl-2-related protein expression and accelerated G1 phase to S phase conversion.