论文部分内容阅读
目的探讨二甲双胍对棕榈酸诱导的脂肪变性成肌细胞内甘油三酯(Triglyceride,TG)含量的影响。方法取Wistar大鼠乳鼠骨骼肌进行原代细胞培养,取第5代成肌细胞,分为5组:对照组(加入正常培养基)、模型组(PA组,加入0.25 mmol/L棕榈酸诱导24 h)、干预组(Met 1、2、3组,加入0.25 mmol/L棕榈酸诱导24 h后,分别加入2.5、5.0和7.5μg/ml的二甲双胍,继续培养24 h)。油红O染色观察细胞内脂滴的变化,计算脂肪变性率;并检测细胞内TG的含量。结果成功建立了成肌细胞脂肪变性模型。模型组较对照组脂变细胞数量明显增多,细胞内TG含量显著增加(P<0.01),而经不同浓度二甲双胍作用后,各干预组脂变细胞数量减少,细胞内TG含量显著下降(P<0.01),与二甲双胍浓度呈正相关。结论二甲双胍可显著减少TG在成肌细胞内的沉积,促进成肌细胞的脂代谢,抑制脂肪变性的形成,具有明显的降脂作用。
Objective To investigate the effect of metformin on triglyceride (TG) content in myogenic stellate cells induced by palmitic acid. Methods Skeletal muscle of Wistar rats was used to culture primary cells. The fifth generation myoblasts were divided into 5 groups: control group (normal medium), model group (PA group, 0.25 mmol / L palmitic acid Induced for 24 h). Met 2, and 2 groups were treated with 0.25, 5.0 and 7.5 μg / ml metformin for 24 h after addition of 0.25 mmol / L palmitic acid for 24 h. The changes of lipid droplets in the cells were observed by oil red O staining, and the rate of fatty degeneration was calculated. The intracellular TG content was also measured. Results Myoblast steatosis model was successfully established. Compared with the control group, the number of adipocytes in the model group increased significantly and the content of TG in the cells increased significantly (P <0.01). After treated with different concentrations of metformin, the number of the lipidated cells decreased and the intracellular TG content decreased significantly (P < 0.01), and the concentration of metformin was positively correlated. Conclusion Metformin can significantly reduce the deposition of TG in myoblasts, promote the lipid metabolism of myoblasts, inhibit the formation of steatosis, and have a significant lipid-lowering effect.