瑞帕利辛改善棕榈酸诱导的骨骼肌细胞胰岛素抵抗  

Reparixin improves palmitic acid-induced insulin resistance in skeletal muscle cells

作　　者：盛菲 倪钰鸽 牛文彦 SHENG Fei;NI Yuge;NIU Wenyan(Department of Immunology,School of Basic Medical Sciences,Tianjin Medical University,Tianjin 300070,China)

机构地区：[1]天津医科大学基础医学院免疫学系,天津300070

出　　处：《天津医科大学学报》2024年第4期338-342,共5页Journal of Tianjin Medical University

基　　金：国家自然科学基金面上项目(82270856)。

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,qPCR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<0.0001),Reparixin逆转PA的影响(F=86.78、264.6,P<0.001,P<0.0001)。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。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 kD(AS160)were detected by Western blotting.The mRNA level of SOCS3 was detected by qPCR.C2C12-GLUT4myc myoblasts were grouped as above.The GLUT4myc translocation was detected by ELISA.Results:CCK-8 results showed that 0,100,200,300μmol/L PA and 0,20,30,40μmol/L Reparixin did not affect C2C12 cell viability.PA reduced insulin-stimulated Akt and AS160 phosphorylation(both P<0.0001),which were reversed by Reparixin(F=86.78,264.6,P<0.001,P<0.0001).PA reduced GLUT4myc translocation(P<0.001)which was reversed by Reparixin(F=41.4,P<0.01).PA increased the levels of SOCS3 mRNA(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 SOCS3 expression.

关 键 词：瑞帕利辛 成肌细胞 胰岛素抵抗 细胞因子信号转导抑制因子3 糖尿病 

分 类 号：R392.1[医药卫生—免疫学]