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GKT137831降低活性氧自由基水平来缓解阿托伐他汀所致的骨骼肌糖摄取下降

GKT137831 alleviates atorvastatin-induced decreased glucose uptake of skeletal muscle by suppressing reactive oxygen species level

    摘要
  • 摘要:
      目的  探讨GKT137831对阿托伐他汀干预骨骼肌细胞的保护作用机制。
      方法  采用阿托伐他汀干预骨骼肌C2C12细胞48 h。采用CCK-8方法分析阿托伐他汀对骨骼肌细胞生存率的影响。采用Western blot检测阿托伐他汀干预后NADPH氧化酶4(Nox4)蛋白表达。采用流式细胞术检测阿托伐他汀对骨骼肌细胞糖摄取及活性氧自由基(ROS)水平的影响。予Nox4抑制剂GKT137831共培养，分析阿托伐他汀对细胞糖摄取及ROS水平的影响。
      结果  阿托伐他汀干预骨骼肌细胞48 h后, C2C12细胞糖摄取能力下降、ROS增加，予GKT137831后可缓解糖摄取下降及ROS增加。CCK-8实验结果显示，阿托伐他汀干预细胞48 h对细胞活力无影响。阿托伐他汀干预C2C12骨骼肌细胞后Nox4表达增加。
      结论  GKT137831通过降低ROS水平来缓解阿托伐他汀所致的骨骼肌糖摄取下降。

     

    Abstract:
      Objective  To explore the mechanism of GKT137831 on protecting skeletal muscle cells by atorvastatin intervention.
      Methods  Atorvastatin was used to intervene C2C12 cells in skeletal muscle for 48 hours. CCK-8 method was used to analyze the effect of atorvastatin on survival rate of skeletal muscle cells. Western blot was used to detect the expression of NADPH Oxidase 4 (Nox4) after atorvastatin intervention. Flow cytometry was used to detect the effect of atorvastatin on glucose uptake and reactive oxygen species (ROS) in skeletal muscle cells. Co-culture of Nox4 inhibitor GKT137831 was used to analyze the effect of atorvastatin on cellular glucose uptake and ROS level.
      Results  After intervention with atorvastatin on skeletal muscle cells for 48 hours, the glucose uptake ability of C2C12 cells decreased and ROS increased. GKT137831 could alleviate the decrease of glucose uptake and the increase of ROS. CCK-8 results showed that atorvastatin had no effect on cell viability after 48 hours of intervention. Nox4 expression increased after atorvastatin intervention on C2C12 skeletal muscle cells.
      Conclusion  GKT137831 can alleviate atorvastatin-induced decreased glucose uptake of skeletal muscle by suppressing reactive oxygen species level.

     

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