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本实验观察十子代平方对原代骨骼肌细胞胰岛素抵抗模型的影响,探讨其改善胰岛素抵抗的作用机制。对原代骨骼肌细胞应用5×10-7mol/L胰岛素干预12 h建立胰岛素抵抗模型,应用十子代平方高、中、低浓度(400、100、25μg/m L)(SZDP-H、SZDP-M、SZDP-L)对造模成功的骨骼肌细胞进行干预,同时另设正常组、模型组,吡格列酮组(40μmol/L)作对照,药物干预24 h后用葡萄糖氧化酶法测定骨骼肌细胞上清液葡萄糖剩余量,采用Western-blot方法测定该方药物干预后骨骼肌细胞AKT、GSK-3β蛋白的表达。实验结果表明十子代平方可以改善骨骼肌细胞胰岛素抵抗模型的葡萄糖代谢,增加AKT和磷酸化位点Ser473蛋白表达,降低GSK-3β蛋白表达,增加其磷酸化位点Ser9蛋白表达。十子代平方可能通过调节AKT/GSK3β通路的机制改善胰岛素抵抗模型骨骼肌细胞的葡萄糖代谢。
In this study, we observed the influence of the tenth generation on the insulin resistance model of primary skeletal muscle cells and the mechanism of insulin resistance. Insulin resistance was induced in primary skeletal muscle cells by 5 × 10-7mol / L insulin for 12 hours. SZDP-H (SZDP-H, SZDP-H, -M, SZDP-L) were used to interfere the successful skeletal muscle cells. At the same time, normal control group, model group and pioglitazone group (40μmol / L) were used as control group. Glucose oxidase method was used to determine skeletal muscle The amount of glucose in the supernatant of the cells was measured by Western-blot. The protein expression of AKT and GSK-3β in the skeletal muscle cells was measured by Western blot. The experimental results show that the SHIJIJQI can improve the glucose metabolism of skeletal muscle insulin resistance model, increase the AKT and phosphorylation site Ser473 protein expression, reduce GSK-3β protein expression and increase the phosphorylation site Ser9 protein expression. The ten generation on behalf of the square may improve the glucose metabolism of insulin resistance model skeletal muscle cells by regulating the mechanism of AKT / GSK3β pathway.