当归多糖对D-半乳糖致衰老小鼠肝损伤的保护作用及其初步机制研究  

Protective effect of Angelica sinensis polysaccharide against liver injury induced by D-galactose in aging mice and its mechanisms

作　　者：夏婕妤 樊艳玲[1] 贾道勇 张梦思[1] 张岩岩[1] 李静[1] 景鹏伟 王璐[1] 王亚平[1] 

机构地区：[1]重庆医科大学干细胞与组织工程研究室、组织胚胎学教研室,400016

出　　处：《中华肝脏病杂志》2016年第3期214-219,共6页Chinese Journal of Hepatology

基　　金：国家自然科学基金（81173398）

摘　　要：目的 研究当归多糖（ASP）对D-半乳糖致衰老小鼠肝脏损伤的保护作用及其初步机制.方法 雄性C57BL/6J小鼠随机分为3组,每组10只.D-半乳糖模型组：小鼠皮下注射D-半乳糖（120mg/kg）,1次/d,持续42d;ASP＋ D-半乳糖模型组：从D-半乳糖模型复制的第8天起,皮下注射ASP （120 mg/kg）,1次/d,持续35 d;正常对照组：小鼠皮下注射等量与等时等渗盐水.药物注射完成第2 d,取眼球血制备血清,检测丙氨酸氨基转移酶（ALT）、天冬氨酸氨基转移酶（AST）、总胆红素（TBil）含量,制备肝脏组织匀浆检测超氧化物歧化酶（SOD）、谷胱甘肽过氧物酶（GSH-Px）、丙二醛（MDA）,晚期糖苷化产物（AGEs）含量.制备肝组织石蜡切片,HE染色观察肝脏病理形态学变化,糖原染色观察肝脏内糖原变化,透射电镜观察肝细胞超微结构.用One-way ANOVA法进行方差分析. 结果 D-半乳糖模型组小鼠肝脏病损严重,肝细胞出现退行性变化.ASP治疗35 d后,ASP＋D-半乳糖模型组与模型组比较,ALT为（21.49±4.81） U/L比（28.29±0.51） U/L,AST为（84.03±9.17） U/L比（97.93±3.56） U/L,TBil为（0.61±0.14）μmol/L比（1.19±0.18）μmol/L;SOD为（170.69±13.41） U/mg比（136.31±21.59） U/mg,MDA为（5.12±1.01）nmol/mg比（8.71±2.04）nmol/mg,GSH-Px为（47.01±8.85） U/ml比（33.22±5.44） U/m1,AEGs的含量下降,肝脏内糖原数量回升,肝脏病损和肝细胞损伤减轻. 结论 ASP能拮抗D-半乳糖所致衰老小鼠肝脏损伤,其机制可能与抑制氧化应激有关.Objective To investigate the protective effect of Angelica sinensis polysaccharide （ASP） against liver injury induced by D-galactose in aging mice and its mechanisms.Methods Male C57BL/6J were randomly divided into three groups with 10 mice in each group.In the D-galactose model group,the mice were subcutaneously injected with D-galactose （120 mg/kg） qd＆#215;42;in the ASP＋D-galactose group,from the 8th day of the establishment of D-galactose model,the mice were subcutaneously injected with ASP （120 mg/kg） qd＆#215;35.In the normal control group,the mice were subcutaneously injected with isotonic saline of the same volume at the same time point.On the 2nd day after the injection was finished,the ocular blood was collected to prepare serum and measure the content of alanine aminotransferase （ALT）,aspartate aminotransferase （AST）,and total bilirubin （TBil）.The liver tissue homogenate was prepared to measure the content of superoxide dismutase （SOD）,glutathione peroxidase （GSH-Px）,malondialdehyde （MDA）,and advanced glycation end products （AGEs）.A paraffin section of liver tissue was prepared;HE staining was performed to observe the pathomorphological changes of the liver,periodic acid-Schiff staining （PAS） was used to observe the changes in glycogen in the liver,and a transrnission electron microscope was used to observe the hepatocyte ultrastructure.Results The D-galactose model group had increased content ofALT,AST,and TBil,reduced activities of SOD and GSH-Px,an increased content of MDA,and severe liver injuries;the hepatocytes showed degenerative changes,the amount of glycogen in the liver decreased,and the accumulation of AGEs increased.The ASP＋D-galactose group had reduced content ofALT,AST,and TBil,increased activities of SOD and GSH-Px,and reduced content of MDA and AGEs;the amount of glycogen in the liver increased,and liver injury and hepatocyte injury were alleviated.Conclusion ASP can antagonize the liver injury induced by D-galactose in aging mice,and it

关 键 词：肝损伤 机制 氧化应激 D-半乳糖 

分 类 号：R285.5[医药卫生—中药学]