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目的:研究氧化应激对高脂高糖饮食诱导的NASH大鼠肝脏损伤的作用,观察复方楂金颗粒剂对NASH的治疗作用,探讨其作用机制。方法:以高脂高糖饮食喂养10周建立NASH大鼠模型,分别以4.032mg.kg-1.d-1、2.016mg.kg-1.d-1、1.008mg.kg-1.d-1的CPZD和69.2mg.kg-1.d-1的易善复进行治疗10周后,观察肝组织病理变化,血清和肝组织MDA含量以及SOD、GSH-PX活性。结果:与正常组相比,模型组大鼠肝脂肪变性、NAFLD活动度积分(NAS)均明显升高(P<0.05),肝组织SOD、GSH-PX活性明显降低而MDA含量明显增加(P<0.05),但血清SOD、GSH-PX活性差异无统计学意义(P>0.05)。改变饮食并应用CPZD治疗后,明显降低NASH大鼠NAS和肝组织MDA含量(P<0.05),升高肝组织SOD、GSH-PX活性(P<0.05),而肝细胞脂肪变性差异无统计学意义(P>0.05)。结论:氧化应激和脂质过氧化是高脂高糖饮食诱导的大鼠发生NASH主要机制,在改变饮食基础上,CPZD不能有效改善肝脂肪变性程度,但明显减轻NASH大鼠的氧化应激,抑制脂质过氧化反应。
Objective: To investigate the effect of oxidative stress on liver injury induced by high-fat and high-sugar diet in NASH rats and to observe the therapeutic effect of compound hawthorn gold granules on NASH and to explore its mechanism. Methods: NASH rat model was established by feeding with high-fat and high-sugar diet for 10 weeks. The rats were fed with 4.032mg.kg-1.d-1,2.016mg.kg-1.d-1, 1.008mg.kg-1.d- 1 CPZD and 69.2mg.kg-1.d-1 for 10 weeks after treatment, observe the pathological changes of liver tissue, serum and liver MDA content and SOD, GSH-PX activity. Results: Compared with the normal group, hepatic steatosis and NAFLD activity index (NAS) in the model group were significantly increased (P <0.05), while the activities of SOD and GSH-PX in the liver tissue were significantly decreased <0.05), but there was no significant difference in serum SOD, GSH-PX activity (P> 0.05). Diet and application of CPZD significantly reduced NAS and rat liver MDA content (P <0.05), increased SOD and GSH-PX activity in liver tissue (P <0.05), while there was no statistical difference in hepatic steatosis Significance (P> 0.05). CONCLUSIONS: Oxidative stress and lipid peroxidation are the main mechanisms of NASH induced by high fat and high glucose diet in rats. CPZD can not effectively improve hepatic steatosis but reduce oxidative stress in NASH rats , Inhibit lipid peroxidation.