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目的:探究木兰醇对胰岛素抵抗的心肌细胞糖代谢的影响。方法:通过MTT法和LDH检测试剂盒检测木兰醇对心肌细胞的细胞毒性;100 n M的胰岛素刺激SD大鼠乳鼠心肌细胞24 h构建心肌胰岛素抵抗模型;葡萄糖检测试剂盒、糖摄取检测试剂盒检测心肌细胞的糖代谢情况;通过Western blot检测糖代谢相关信号通路蛋白磷酸化AKT的表达情况。结果:木兰醇对心肌细胞无明显毒性,且剂量依赖性的增加胰岛素敏感和非敏感型心肌细胞糖代谢。30μM的木兰醇孵育心肌细胞1 h,显著激活细胞磷酸化AKT信号通路。100 n M的胰岛素刺激心肌细胞24 h后,再次给予100 n M的胰岛素刺激后,心肌细胞的糖代谢水平无明显变化。30μM的木兰醇孵育心肌细胞24 h显著增加胰岛素抵抗心肌细胞的糖代谢水平。PI3K抑制剂Wortmanmin完全抑制木兰醇的上述作用。结论:木兰醇可通过激活AKT信号通路改善心肌细胞胰岛素抵抗。
Objective: To investigate the effect of magnolol on glucose metabolism in insulin-resistant cardiomyocytes. Methods: The cytotoxicity of magnolol on cardiomyocytes was detected by MTT assay and LDH assay kit. Cardiac insulin resistance was induced by 100 nM insulin for 24 h in neonatal rat cardiomyocytes. Glucose assay kit, The expression of phosphorylated AKT in glucose metabolism related signaling pathway was detected by Western blot. Results: Magnolyn did not show obvious cytotoxicity on cardiomyocytes and increased the glucose metabolism of insulin-sensitive and non-sensitive cardiomyocytes in a dose-dependent manner. 30μM magnolol incubated cardiomyocytes for 1 h, significantly activating the phosphorylated AKT signaling pathway. Cardiac myocytes were stimulated by 100 nM insulin for 24 h, but there was no significant change in myocardial glucose metabolism after 100 nM insulin stimulation. Incubation of 30μM magnolol for 24 h significantly increased the glucose metabolism of insulin resistant cardiomyocytes. The PI3K inhibitor Wortmanmin completely inhibits the above effects of magnolol. Conclusion: Magnolyn can improve cardiomyocyte insulin resistance by activating AKT signaling pathway.