血管紧张素Ⅱ对人肝癌细胞株HepG2细胞葡萄糖代谢的影响及缬沙坦干预作用的研究

摘要

Objective To investigate the effect of ATⅡ on glucose metabolism in HepG2 cells,and to observe the intervention of valsartan on it.Methods Different concentrations of AT Ⅱ (10-9 ～10-5mol/L) were added into the cultured HepG2 cells for different times,and the amount of glucose consumption was measured.The time and concentration of AT Ⅱ affecting glucose metabolism were determined.Then the HepG2 cells were randomized into the control group,AT Ⅱ group,and valsartan pretreated group.The glycogenesis,gluconeogenesis and glycolysis in HepG2 cells were measured.Resnlts The best time and concentration of ATⅡ were at 36 h and 10-6mol/L.ATⅡ decreased glucose consumption through decreasing the glycogenesis and lactic acid production and increasing gluconeogenesis,while no significant impact on pyruvate kinase activity.Valsartan could antagonize AT Ⅱ's effect mainly through the inhibition of gluconeogenesis and promotion of glycogenesis.Conclusion Valsartan can reverse the effect of AT Ⅱ on glucose metabolism,providing a theoretical basis for the prevention and treatment of diabetes.%目的 研究ATⅡ对人肝癌细胞株HepG2细胞葡萄糖代谢的影响,并探讨缬沙坦在该过程中的干预作用. 方法 体外培养HepG.2细胞,分别加入10-9～10-5 mol/L的ATⅡ作用不同时间,确定对细胞葡萄糖消耗量影响最明显的ATⅡ浓度和作用时间.将HepG2细胞随机分为对照组、ATⅡ组、缬沙坦干预组,测定细胞葡萄糖消耗量、糖原合成量、糖异生量及糖酵解的指标. 结果 10-6 mol/L的ATⅡ作用HepG2细胞36 h,葡萄糖消耗量减少最明显(P＜0.01).ATⅡ作用后,细胞糖原合成量、乳酸生成量下降(P＜0.05),糖异生量增加(P＜0.05),丙酮酸激酶活力差异无统计学意义(P＞0.05)；缬沙坦干预后,糖异生量减少(P＜0.05),糖原合成量增加(P＜0.05). 结论 缬沙坦可逆转ATⅡ所致的HepG2细胞葡萄糖代谢异常,为糖尿病预防及治疗提供参考.