目的 通過體外實驗探討羈糖脂改善2型糖尿病胰島素抵抗（IR）的作用，并初步探明其作用機制。方法 采用1×10^-7 mol/L胰島素誘導HepG2細胞，建立IR細胞模型；MTT法檢測羈糖脂對HepG2細胞的增殖抑制率；葡萄糖氧化酶-過氧化物酶（GOD-POD）法檢測羈糖脂對HepG2 IR細胞葡萄糖吸收的影響；Western blotting法檢測胰島素受體底物1磷酸化絲氨酸p-IRS-1（Ser307）、磷酸酰肌醇-3-激酶（PI3K）、葡萄糖轉運體-4（GLUT-4）的表達。結果 HepG2細胞置于含10^-7胰島素培養(yǎng)液孵育24 h，與對照組比較，葡萄糖吸收水平下降，表明建模成功；30～120 μg/mL羈糖脂均能顯著增加IR細胞葡萄糖吸收率，顯著上調GLUT-4、PI3K蛋白表達水平，顯著下調IRS-1 Ser307磷酸化水平。結論 羈糖脂能有效增強HepG2 IR細胞對葡萄糖的消耗能力，推測與上調GLUT-4、PI3K蛋白表達，抑制IRS-1絲氨酸磷酸化相關。

Objective To evaluate the effect of Ji Tang Zhi on glucose metabolism in insulin resistance (IR) HepG 2 cell line, and to explore the related mechanism. Methods The HepG2 cells were incubated in culture medium addition of 10^-7 mol/L insulin for 24 h to establish the IR cell model. Effect of Ji Tang Zhi on rate of glucose absorption in HepG2 cell was detected by the method of glucose oxidase-peroxidase (GOD-POD). We performed an MTT assay to determine cytotoxicity effects of Ji Tang Zhi on HepG2 cell line. The expression of p-IRS-1 Ser307, PI3K and GLUT-4 were detected by Western blotting. Results Incubated with 10^-7 mol/L insulin for 24 h, the insulin resistance cell model had been built. Compared with model group, the rate of glucose absorption of cell treated with JTZ (30 ~120 μg/mL) was significantly improved. According to model cells, the expression of GLUT-4 and PI3K decreased significantly compared to control cells. While the expression of p-IRS-1 Ser 307 was inhibited and GLUT-4 and PI3K expression were increased in IR cells after treated with JTZ (30 ~120 μg/mL). Conclusion JTZ exert beneficial effects on hyperglycosemia in IR cell line possibly through regulating the levels of GLUT-4, p-IRS-1 Ser307 and PI3K in HepG2 cell.

淮安市科技局基金資助項目（HAN2015025）