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目的探讨碳水化合物反应元件结合蛋白(Carbohydrate response element binding protein,ChREBP)在高糖诱导肝细胞脂变中的作用。方法分别以18和25 mmol/L葡萄糖培养L02细胞,以11 mmol/L葡萄糖培养L02细胞作为对照,甘油三酯(TG)含量测定及油红O染色观察细胞脂变程度;免疫荧光观察细胞ChREBP的核转位情况;RT-PCR检测细胞肝型丙酮酸激酶(Liver pyruvate kinase,LPK)基因mRNA的表达水平,Western blot分析细胞脂肪酸合成酶(Fatty acid synthase,FAS)蛋白的表达水平。结果与对照组比较,高糖可使L02细胞内甘油三酯和脂滴含量增加,刺激ChREBP核转位,上调LPK基因mRNA和FAS蛋白的表达水平。结论葡萄糖可能通过其代谢产物经ChREBP-LPK-FAS途径诱导肝细胞脂肪变性。
Objective To investigate the role of carbohydrate response element binding protein (ChREBP) in the induction of hepatocellular lipid hyperlipemia. Methods L02 cells were cultured with 18 and 25 mmol / L glucose, L02 cells were cultured with 11 mmol / L glucose as control, triglyceride (TG) content and oil red O staining were observed. The expression of ChREBP . The expression of LPK gene mRNA was detected by RT-PCR and the expression of fatty acid synthase (FAS) protein was analyzed by Western blot. Results Compared with the control group, high glucose increased the triglyceride and lipid droplets in L02 cells, stimulated the nuclear translocation of ChREBP and up-regulated the expression of LPK mRNA and FAS protein. Conclusion Glucose may induce hepatic steatosis through ChREBP-LPK-FAS pathway through its metabolites.