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目的通过体外实验探讨羁糖脂改善2型糖尿病胰岛素抵抗(IR)的作用,并初步探明其作用机制。方法采用1×10-7 mol/L胰岛素诱导Hep G2细胞,建立IR细胞模型;MTT法检测羁糖脂对Hep G2细胞的增殖抑制率;葡萄糖氧化酶-过氧化物酶(GOD-POD)法检测羁糖脂对Hep G2 IR细胞葡萄糖吸收的影响;Western blotting法检测胰岛素受体底物1磷酸化丝氨酸p-IRS-1(Ser307)、磷酸酰肌醇-3-激酶(PI3K)、葡萄糖转运体-4(GLUT-4)的表达。结果 Hep G2细胞置于含10-7胰岛素培养液孵育24 h,与对照组比较,葡萄糖吸收水平下降,表明建模成功;30~120μg/m L羁糖脂均能显著增加IR细胞葡萄糖吸收率,显著上调GLUT-4、PI3K蛋白表达水平,显著下调IRS-1 Ser307磷酸化水平。结论羁糖脂能有效增强Hep G2 IR细胞对葡萄糖的消耗能力,推测与上调GLUT-4、PI3K蛋白表达,抑制IRS-1丝氨酸磷酸化相关。
OBJECTIVE: To explore the effect of diabetes mellitus (DM) on insulin resistance (IR) in type 2 diabetes mellitus (T2DM) in vitro and to explore its mechanism of action. Methods Hep G2 cells were induced by 1 × 10-7 mol / L insulin and IR cell model was established. The inhibitory rate of proliferation of Hep G2 cells was detected by MTT assay. The glucose oxidase-peroxidase (GOD-POD) The effect of blood sugar on the glucose uptake in Hep G2 IR cells was examined by Western blotting. The effects of insulin receptor substrate 1 phosphorylation serine p-IRS-1 (Ser307), phosphoinositide 3-kinase (PI3K) Body-4 (GLUT-4) expression. Results Hep G2 cells were incubated in medium containing 10-7 insulin for 24 h. Compared with the control group, the glucose uptake of Hep G2 cells was decreased, indicating that the model was successfully established. Glucose uptake of IR cells could be significantly increased by 30 ~ 120 μg / , Significantly up-regulated GLUT-4 and PI3K protein expression, and significantly decreased IRS-1 Ser307 phosphorylation. Conclusion Conjugated lipopolysaccharide can effectively enhance the glucose-depleting capacity of Hep G2 IR cells, which is presumed to be related to up-regulation of GLUT-4 and PI3K protein expression and inhibition of IRS-1 serine phosphorylation.