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目的:基于蛋白磷酸酶(PP1)-DNA依赖的蛋白激酶(DNA-PK)-上游刺激因子1(USF1)信号通路,探讨中药组分HJJB方防治非酒精性脂肪肝(NAFLD)的作用机制。方法:采用高脂饮食诱导的大鼠NAFLD模型。设模型组、HJJB方组和罗格列酮组,分别灌胃给药6周。HE染色观察肝组织病理变化;测定肝组织甘油三酯(TG)、游离脂肪酸(FFA)含量的变化;肝组织PP1、DNA-PK、USF1 m RNA水平和蛋白含量的变化。结果:模型组肝组织出现显著的肝细胞脂肪变性及空泡样变,肝组织TG、FFA含量较正常组显著升高(P<0.01),肝组织PP1、DNA-PK、USF1 m RNA水平和蛋白含量较正常组均明显升高(P<0.01)。HJJB方组的上述病理改变明显减轻,肝组织TG、FFA含量较模型组显著降低(P<0.01),肝组织PP1、DNA-PK、USF1 m RNA水平和蛋白含量较模型组显著降低(P<0.01)。结论:HJJB方能显著降低脂肪肝大鼠肝组织PP1 m RNA水平和蛋白含量,进而抑制其下游信号通路,这可能是其防治NAFLD的重要机制。
OBJECTIVE: To investigate the mechanism of Chinese medicine HJJB in preventing and treating non-alcoholic fatty liver (NAFLD) based on the signal transduction pathway of protein phosphatase (PP1) -DNA dependent protein kinase (USP1). Methods: A rat model of NAFLD induced by high fat diet was used. The model group, HJJB group and rosiglitazone group were administered orally for 6 weeks. The pathological changes of liver tissue were observed by HE staining. The content of triglyceride (TG) and free fatty acid (FFA) in liver tissues were measured. The changes of PP1, DNA-PK, USF1 m RNA and protein content were observed. Results: The hepatic steatosis and vacuolar degeneration were observed in the model group. The levels of TG and FFA in the liver tissue were significantly increased (P <0.01), the levels of PP1, DNA-PK and USF1 mRNA in the liver tissue were significantly increased Protein levels were significantly higher than the normal group (P <0.01). Compared with model group, the contents of TG and FFA in liver tissue of HJJB group were significantly reduced (P <0.01), and the levels of PP1, DNA-PK and USF1 mRNA in liver tissue were significantly lower than those in model group (P < 0.01). Conclusion: HJJB can significantly reduce the level of PP1mRNA and the protein content in hepatic tissue of fatty liver rats, and then inhibit its downstream signaling pathway, which may be an important mechanism of its prevention and treatment of NAFLD.