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目的:观察黄芪提取物对非酒精性脂肪性肝病大鼠的作用及其可能机制。方法:应用高脂饮食复制大鼠非酒精性脂肪性肝病模型。雄性Wister大鼠40只,随机分为正常对照组(A组)、模型组(B组)、低剂量黄芪组(C组)、中剂量黄芪组(D组)和高剂量黄芪组(E组),每组各8只。药物干预组大鼠在进行高脂饮食同时每日给予不同剂量黄芪提取物灌胃,药物干预10周末结束实验,检测肝组织甘油三酯和总胆固醇,肝组织氧化指标丙二醛(MDA)含量,超氧化物歧化酶(SOD)活力;血清丙氨酸转移酶(ALT)、门冬氨酸转移酶(AST)、甘油三酯(TG)、总胆固醇(TC)、低密度脂蛋白(LDL)、空腹血糖(FBG),并观察肝脏的病理改变。结果:与正常对照组相比,模型组大鼠病理显示脂肪变性、炎症或炎症坏死并伴有血清ALT、AST、TC、LDL、FBG及肝组织TG、TC和MDA明显升高,而肝组织SOD活性明显降低。药物干预组大鼠血清ALT、AST、TC、LDL、FBG和肝组织TG、TC和MDA降低,而肝组织SOD活性升高,且肝脏脂肪变性和炎症坏死程度减轻(P<0.01,P<0.05)。结论:黄芪提取物对大鼠高脂饮食诱导的非酒精性脂肪性肝病有防治作用,其机制可能与提高抗氧化能力相关。
Objective: To observe the effect of astragalus extract on non-alcoholic fatty liver disease and its possible mechanism. Methods: A rat model of nonalcoholic fatty liver disease was induced by high fat diet. Forty male Wister rats were randomly divided into normal control group (group A), model group (group B), low dose Astragalus group (group C), medium dose Astragalus group (group D) and high dose Astragalus group (group E) ), Each group of 8. Rats in the drug-treated group were given high-fat diet and different doses of astragalus extract were intragastrically administered daily. At the end of the 10-week drug intervention, the triglyceride and total cholesterol in the liver tissue and the content of malondialdehyde (MDA) , Superoxide dismutase (SOD), serum ALT, AST, TG, TC, LDL ), Fasting blood glucose (FBG), and observe the pathological changes of the liver. Results: Compared with the normal control group, the pathological changes in the model group showed steatosis, inflammatory or inflammatory necrosis accompanied by serum ALT, AST, TC, LDL, FBG and liver tissue TG, TC and MDA significantly increased, while the liver tissue SOD activity was significantly reduced. The levels of ALT, AST, TC, LDL, FBG and TG, TC and MDA in the liver of the rats in the drug-treated group were decreased, while the activity of SOD in the liver tissue was increased, and the degree of hepatic steatosis and inflammatory necrosis was also alleviated (P <0.01, P <0.05 ). Conclusion: The extract of Astragalus can prevent and treat non-alcoholic fatty liver disease induced by high-fat diet in rats, and its mechanism may be related to the enhancement of antioxidant capacity.