中文摘要：

目的探讨丹参酮Ⅰ对HepG2细胞胰岛素抵抗的作用及分子机制。方法高浓度胰岛素诱导建立胰岛素抵抗HepG2细胞模型;MTT法确定丹参酮Ⅰ的给药浓度;葡萄糖氧化酶法检测丹参酮Ⅰ对胰岛素抵抗HepG2细胞葡萄糖消耗量的影响;Western blot法测定蛋白络氨酸磷酸酶1B（PTP1B）、磷酸化的丝氨酸/苏氨酸蛋白激酶B（P-AKT）、丝氨酸/苏氨酸蛋白激酶B（AKT）蛋白表达情况。结果以10^-7mol/L胰岛素诱导24 h成功建立了胰岛素抵抗HepG2细胞模型;MTT筛选出了78、156、312 ng/ml丹参酮Ⅰ给药浓度;丹参酮Ⅰ呈浓度依赖地增加胰岛素抵抗HepG2细胞葡萄糖消耗量;Western blot法结果显示,与正常组比较,模型组PTP1B表达升高、P-AKT表达降低。与模型组比较,丹参酮Ⅰ给药组PTP1B的表达浓度依赖性地降低、P-AKT的表达浓度依赖性地升高。结论丹参酮Ⅰ能改善胰岛素抵抗HepG2细胞,其机制可能是通过抑制PTP1B的表达,进而促进了P-AKT/AKT信号通路的活化。

英文摘要：

Objective To explore effect and molecular mechanism of improved insulin resistance（ IR） in Hep G2 cells by tanshinone Ⅰ. Methods IR-Hep G2 was induced by high concentrations of insulin. The appropriate concentrations of tanshinone Ⅰ were determined by MTT assay. The glucose consumption was detected by glucose assay kit. The expressions of protein tyrosine phosphatase 1B（ PTP1B）,P-AKT,AKT were determined by Western blot. Results The IR-Hep G2 cells were established successfully by incubating with 10- 7mol / L insulin for 24 hours. The ultimate concentrations of tanshinone Ⅰ were determined as 78,156,312 ng / ml and tanshinone Ⅰconcentration-dependently increased glucose consumption of IR-Hep G2 cells. Western blot showed increased expression of PTP1 B and decreased expression of P-AKT in model group compared with the normal group. Moreover,tanshinone Ⅰ concentration-dependently decreased expression of PTP1 B and increased expression of P-AKT compared with the model group. Conclusion Tanshinone Ⅰ improved IR in Hep G2 cells. The putative mechanism is that tanshinone Ⅰ decrease expression of PTP1 B and promotes activation of P-AKT / AKT signaling pathway.