摘要
目的：研究黄芪甲苷对铁超载造成肝损伤保护的作用机制。方法：小鼠按体质量随机分为空白组,模型组、黄芪甲苷（As）低、中、高剂量组。连续给药45 d,取血清,检测血清Fe,总铁结合力（total iron binding capacity,TIBC）,丙氨酸氨基转移酶（glutamic-pyruvic transaminase,ALT）,天门冬氨酸氨基转移酶（glutamic oxalacetic transaminase,AST）,总胆红素（total bilirubin,T-BIL）,丙二醛（malondialdehyde,MDA）,谷胱甘肽（glutathione,GSH）水平;用苏木素-伊红（HE）染色观察肝脏病理组织学变化;用免疫组化法分析肝脏组织蛋白硝化的表达变化;用原位末端转移酶标记技术（TUNEL）染色法观察肝细胞凋亡的变化。结果：与空白组比较,模型组小鼠血清中血清Fe,ALT,AST,MDA,肝中铁和T-BIL含量显著增加（P〈0.01）,而TIBC和GSH含量显著降低（P〈0.05,P〈0.01）;与模型组比较,黄芪甲苷组小鼠血清中血清Fe,ALT,AST,MDA水平,及肝中Fe和TBIL含量显著降低（P〈0.05,P〈0.01）,肝中TIBC和GSH含量显著增高（P〈0.05,P〈0.01）;HE结果显示,与空白组比较,铁超载组可见肝细胞水样变性、肝细胞脂肪变性和炎症细胞浸润等;不同浓度黄芪甲苷组的上述病理改变得以改善;免疫组化结果发现,与空白组比较,铁超载组血管周围细胞浆中3-硝基酪氨酸（3-NT）显著增加,而黄芪甲苷组血管膜周围的3-硝基酪氨酸则显著减少;TUNEL染色发现与空白组比较,模型组肝细胞凋亡显著增多;与模型组比较,黄芪甲苷组肝细胞凋亡显著减少。结论：黄芪甲苷对铁超载造成的肝损伤具有保护作用。
Objective： To investigate the protective role of astragaloside（As） in the liver injury caused by iron overload. Method： The mice were randomly divided into blank control group,model group,as low-dose group,as middle-dose group and as high-dose group according to their weight. Mice were intraperitoneally injected with As once daily for 45 d. Then their serum was taken to determine the content of serum iron,total iron binding capacity（TIBC）,alanine aminotransferase（ALT）,aspartate aminotransferase（AST）,total bilirubin（T-BIL）,malondialdehyde（MDA）,and glutathione（GSH）; pathological changes in liver tissues were examined by hematoxylin-eosin（HE） staining; the expression changes of protein nitration in liver tissues were detected by immunohistochemical staining; and the changes of the liver apoptosis were observed by Td T-mediated d UTP nick end labeling（TUNEL） staining. Result： As compared with the blank group,the levels of serum Fe,MDA,ALT,and AST in serum as well as Fe and T-BIL in liver were increased in the model group（P〈0. 01）,while the levels of GSH and TIBC were decreased significantly（P〈0. 05,P〈0. 01）. However,as compared with the model group,the levels of serum Fe,MDA,ALT and AST in serum as well as Fe and T-BIL levels in liver were significantly decreased in the As groups（P〈0. 05,P〈0. 05）,while the levels of GSH and TIBC in liver were significantly decreased（P〈0. 05,P〈0. 01）. HE results showed that as compared with blank group,hepatocyte hydropic degeneration,hepatocyte fatty degeneration and inflammatory cell infiltration were present in iron overload group; but these pathological damages were improved in different dose As groups. Immunohistochemical results showed that as compared with the blank group,the 3-nitrotyrosine（3-NT） level in the perivascular plasma was increased significantly in the iron overload group,but was significantly reduced in the As groups. TUNEL staining results showed that as compared with the blank group,hepatocyte apoptosis was significantly increased in model group; as compared with the model group,the hepatocyte apoptosis was significantly reduced in As groups.Conclusion： As could attenuate the liver injury induced by iron overload.
作者
叶枝红
谢海纳
钱知知
叶晶
姜文静
刘霖
谢东浩
张良
YE Zhi-hong;XIE Hai-na;QIAN Zhi-zhi;YE Jing;JIANG Wen-jing;LIU Lin;XIE Dong-hao;ZHANG Liang(School of Pharmacy, Jiangsu University, Zhenjiang 212013, China;School of Basic Medical Sciences, Nanfing University of Chinese Medicine, Nanfing 210023, China;School of Pharmacy, Nanfing University of Chinese Medicine, Nanjing 210023, China;Dahua Hospital of Xuhui District, Shanghai 200237, China)
出处
《中国实验方剂学杂志》
CAS
CSCD
北大核心
2018年第8期116-121,共6页
Chinese Journal of Experimental Traditional Medical Formulae
基金
上海市徐汇区医学科研项目(SHXH201310)
关键词
黄芪甲苷
铁超载
肝损伤
凋亡
astragaloside
iron overload
liver injury
apoptosis
