【摘要】 目的：探讨瑞帕利辛（Reparixin）对棕榈酸（PA）诱导的C2C12成肌细胞胰岛素抵抗的影响。方法：CCK-8(cell counting Kit-8)法检测不同浓度的PA或Reparixin处理后C2C12成肌细胞活力；将C2C12成肌细胞分为牛血清白蛋白组（BSA组）、PA组、PA+Reparixin组，免疫印迹检测SOCS3蛋白水平及胰岛素信号分子蛋白激酶B(Akt)和160 kD的蛋白激酶B底物（AS160）磷酸化水平，q PCR检测SOCS3 mRNA水平。将C2C12-GLUT4myc小鼠成肌细胞同上分组，ELISA检测细胞GLUT4myc转位。结果：0、100、200、300μmol/L的PA和0、20、30、40μmol/L的Reparixin均不影响C2C12细胞活力。PA降低胰岛素磷酸化Akt和AS160的作用（均P<0.000 1）,Reparixin逆转PA的影响（F=86.78、264.6,P<0.001,P<0.000 1）。PA降低胰岛素促进GLUT4myc转位的作用（P<0.001）,Reparixin逆转PA的影响（F=41.4,P<0.01）。PA上调SOCS3 mRNA(P<0.001)和蛋白水平（P<0.05）,Reparixin逆转PA对SOCS3的影响（F=51.64、7.97,P<0.001,P<0.05）。结论：Reparixin可能通过下调SOCS3基因和蛋白表达，缓解棕榈酸诱导的小鼠C2C12成肌细胞胰岛素抵抗。更多还原

【Abstract】 Objective:To investigate the effect of Reparixin on palmitic acid(PA)-induced insulin resistance in C2C12 myoblasts.Methods:The cell counting Kit-8(CCK-8)was used to detect the viability of C2C12 myoblasts treated with different concentrations of PA and Reparixin. C2C12 myoblastes were divided into bovine serum albumin group(BSA group),PA group and PA+Reparixin group,respectively. The expressions of suppressor of cytokine signaling 3(SOCS3)and the phosphorylation of insulin signaling molecules protein kinase B(Akt),protein kinase B substrate of 160 k D(AS160)were detected by Western blotting. The m RNA level of SOCS3was detected by qPCR. C2C12-GLUT4mycmyoblasts were grouped as above. The GLUT4myctranslocation was detected by ELISA.Results:CCK-8 results showed that 0,100,200,300 μmol/L PA and 0,20,30,40 μmol/L Reparixin did not affect C2C12 cell viability.PA reduced insulin-stimulated Akt and AS160 phosphorylation(bothP<0.000 1),which were reversed by Reparixin(F=86.78,264.6,P<0.001,P<0.000 1). PA reduced GLUT4myctranslocation(P<0.001)which was reversed by Reparixin(F=41.4,P<0.01). PA increased the levels of SOCS3 m RNA(P<0.001)and SOCS3 protein(P<0.05),which were reversed by Reparixin(F=51.64,7.97,P<0.001,P<0.05).Conclusion:Reparixin may alleviate PA-induced insulin resistance in C2C12 myoblasts by down-regulating SOCS3expression.更多还原