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当归多糖治疗小鼠乙醇性肝损伤中丙二醛、超氧化物歧化酶及谷胱甘肽过氧化物酶的变化及意义 被引量:12

Effect of Angelica sinensis polysaccharide on serum malondialdehyde,superoxide dismutase and glutathione peroxidase of alcohol-induced hepatic injured mice
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摘要 目的:探讨当归多糖治疗小鼠乙醇性肝损伤中丙二醛(MDA)、超氧化物歧化酶(SOD)及谷胱甘肽过氧化物酶(GSHPx)的变化及意义。方法:通过一次性高浓度乙醇灌胃建立小鼠乙醇性肝损伤模型,之后连续腹腔注射当归多糖6 d,血清生化检测MDA、SOD及GSH-Px,光镜观察肝形态结构变化。结果:小鼠乙醇性肝损伤后,血清MDA显著增高,SOD及GSH-Px显著下降,同时肝组织结构呈弥漫性脂肪变性损伤。用当归多糖治疗后,伴随肝组织结构的修复,血清MDA显著下降,SOD及GSH-Px增高。结论:当归多糖可通过阻断膜脂质过氧化起到保护肝细胞的作用,血清MDA、SOD及GSHPx水平的变化对判断肝的损害程度、病情发展、评估预后有一定的意义。 Objective: To explore the effect of Angelica sinensis polysaccharide on expressions of malondialdehyde(MDA), superoxide dismutase (SOD)and glutathione peroxidase (GSH-Px) in alcohol injured mouse livers and its significance. Methods: A mouse model of acute alcoholic liver injury was established by a one-time garage of high concentration of alcohol. The general situation of the mice was then observed by intraperitoneal injection of Angelica sinensis polysaccharides for 6 days. The changes of MDA, SOD and GSH-Px in serum biochemistry were detected in different conditions. Changes of liver morphology and structure were observed with light microscope. Results: After alcoholic liver injury in mice, serum MDA increased significantly, and SOD and GSH-Px decreased significantly. At the same time, the liver tissue showed diffuse steatosis. After being treated with Angelica sinensis polysaccharide, along with the structure of the liver tissue repair, serum MDA decreased significantly, and SOD and GSH-Px increased. Conclusion : Angelica sinensis polysaccharide enable to protect the hepatocytes by blocking lipid peroxidation. And, serum MDA, SOD and GSH-Px could be used to biomarkers for hepatic injury, progression and outcomes.
出处 《解剖学杂志》 CSCD 北大核心 2017年第4期382-385,共4页 Chinese Journal of Anatomy
基金 长治医学院科技创新团队项目(CX201415) 山西省大学生创新创业项目(2014301)
关键词 当归多糖 丙二醛 超氧化物歧化酶 谷胱甘肽过氧化物酶 肝损伤 小鼠 Angelica sinensis polysaccharide malondialdehyde superoxide dismutase glutathione peroxidase liver injury mouse
作者简介 第1作者E-mail:905066445@qq.com
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