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目的:研究乙肝Ⅱ号对实验性明显肝损伤小鼠抗自由基的作用及其机制。方法:采用四氯化碳(CCl_4)慢性肝损伤模型,观察小鼠肝组织匀浆丙二醛(MDA)含量,超氧化物岐化酶(SOD)及谷胱甘肽过氧化物酶(FSH-PX)活力的改变,以及乙肝Ⅱ号对MDA、SOD和GSH-PX变化的影响。结果:乙肝Ⅱ号防治组与模型相比,肝损伤明显减轻,肝匀浆MDA含量下降,SOD活力上升,GSH-PX活力上升,变化的程度与用药量呈明显的量效关系,且抗自由基作用优于乙肝宁冲剂。结论:乙肝Ⅱ号对实验性慢性肝损伤小鼠具有抗自由基损伤的作用。
Objective: To study the effect and mechanism of hepatitis B II on free radicals in mice with experimental hepatic injury. METHODS: Chronic liver injury model with carbon tetrachloride (CCl_4) was used to observe the content of malondialdehyde (MDA), superoxide dismutase (SOD) and glutathione peroxidase (FSH) in liver homogenate of mice. -PX) changes in viability, and the effect of hepatitis B II on changes in MDA, SOD, and GSH-PX. Results:Compared with the model, compared with the control group of hepatitis B, the liver injury was significantly reduced, the content of MDA in liver homogenate was decreased, the activity of SOD was increased, and the activity of GSH-PX was increased. The degree of change and dosage were significant in a dose-effect relationship, and the anti-free The base effect is better than Yiganning Granules. Conclusion: Hepatitis B II has anti-free radical damage effect on experimental chronic liver injury mice.