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双氢睾酮逆转棕榈酸诱导的小鼠骨骼肌细胞胰岛素抵抗及其机制
引用本文:齐睿,牛文彦.双氢睾酮逆转棕榈酸诱导的小鼠骨骼肌细胞胰岛素抵抗及其机制[J].天津医科大学学报,2022,0(2):140-144.
作者姓名:齐睿  牛文彦
作者单位:(天津医科大学基础医学院免疫学系,天津300070)
摘    要:目的:探讨双氢睾酮(DHT)对棕榈酸(PA)诱导的C2C12小鼠骨骼肌细胞胰岛素抵抗的影响及其分子机制。方法:分别用牛清蛋白(BSA)、PA或PA+DHT孵育C2C12细胞24 h,Western印迹检测胰岛素信号通路蛋白激酶B(Akt)、Akt底物AS160以及炎症相关蛋白核因子κB抑制蛋白(IκB)激酶(IKK)、核因子κB(NF-кB)的磷酸化水平、促炎细胞因子白细胞介素-6(IL-6)、肿瘤坏死因子-α(TNF-α)蛋白水平,qPCR检测IL-6和TNF-α mRNA水平。结果:Western印迹结果显示,PA降低胰岛素刺激的Akt、AS160磷酸化水平(均P<0.05);DHT逆转PA对胰岛素刺激的Akt和AS160磷酸化的抑制作用(F=59.29、7.829;均P<0.05)。PA升高IKK和NF-κB磷酸化水平(均P<0.05)及IL-6和TNF-α蛋白表达(均P<0.01);DHT降低PA升高的IKK、NF-κB磷酸化水平(F=13.94、10.65,均P<0.05)和IL-6和TNF-α蛋白表达(F=10.82、15.14,均P<0.05)。qPCR结果显示,PA可升高IL-6、TNF-α mRNA水平(均P<0.01);DHT降低IL-6和TNF-α mRNA的表达(F=13.71、12.77;均P<0.05)。结论:DHT可能通过抑制PA诱导的C2C12骨骼肌细胞炎症信号,改善PA诱导的胰岛素抵抗。

关 键 词:双氢睾酮  骨骼肌  胰岛素抵抗  炎症  糖尿病

Palmitic acid-induced insulin resistance in mouse skeletal muscle cells reversed by dihydrotestosterone and its mechanism
QI Rui,NIU Wen-yan.Palmitic acid-induced insulin resistance in mouse skeletal muscle cells reversed by dihydrotestosterone and its mechanism[J].Journal of Tianjin Medical University,2022,0(2):140-144.
Authors:QI Rui  NIU Wen-yan
Affiliation:(Department of Immunology,School of Basic Medical Sciences,Tianjin Medical University,Tianjin 300070,China)
Abstract:Objective: To investigate the effect of dihydrotestosterone (DHT) on palmitic acid(PA)-induced insulin resistance in C2C12 murine skeletal muscle cells and its potential molecular mechanism. Methods:C2C12 cells were incubated with bovine albumin (BSA),PA or PA+DHT for 24 hours. The phosphorylation levels of insulin signaling pathway related protein Akt,Akt substrate AS160 and inflammatory related protein IκB kinase(IKK),nuclear factor κB(NF-кB),pro-inflammatory cytokine interleukin-6(IL-6) and tumor necrosis factor-α(TNF-α) were detected by Western blotting.The mRNA levels of IL-6 and TNF-α were detected by qPCR. Results:Western blotting results showed that PA reduced insulin-stimulated Akt and AS160 phosphorylation levels(all P<0.05). DHT reversed the inhibitory effect of PA on insulin-stimulated Akt and AS160 phosphorylation(F=59.29,7.829;all P<0.05).PA increased the phosphorylation levels of IKK and NF-κB(all P<0.05) and the protein expression of IL-6 and TNF-α(all P<0.01). DHT decreased the phosphorylation levels of IKK and NF-κB(F=13.94,10.65;all P<0.05) and the expression of IL-6 and TNF-α(F=10.82,15.14;all P<0.05). The qPCR results showed that PA increased IL-6 and TNF-α mRNA level(both P <0.01);DHT reduced the mRNA levels of IL-6 and TNF-α(F=13.71,12.77;both P<0.05). Conclusion:DHT may reverse PA-induced insulin resistance by inhibiting inflammation signal in C2C12 skeletal muscle cells.
Keywords:dihydrotestosterone  skeletal muscle  insulin resistance  inflammation  diabetes mellitus
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