| 引用本文: |
白雪,陆璐,刘振权,边艳琴.黄芪甲苷抗二甲基亚硝胺诱导肝纤维化大鼠效应研究[J].湖南中医药大学学报,2020,40(1):22-27[点击复制] |
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| 黄芪甲苷抗二甲基亚硝胺诱导肝纤维化大鼠效应研究 |
| 白雪,陆璐,刘振权,边艳琴 |
| (北京中医药大学, 北京 100029;北京积水潭医院, 北京 100035;上海中医药大学, 上海 201203;上海市光华中西医结合医院, 上海 200052) |
| 摘要: |
| 目的 探讨黄芪甲苷对二甲基亚硝胺（Dimethylnitrosamine，DMN）诱导肝纤维化大鼠模型的作用。方法 选取27只雄性Wistar大鼠，随机分为正常组、模型组和黄芪甲苷组。模型组和黄芪甲苷组大鼠，采用腹腔注射DMN诱导肝纤维化模型，持续4周。于造模第3周开始，黄芪甲苷组在继续造模的同时予以黄芪甲苷干预，正常组和模型组给于等容量蒸馏水灌胃。4周末（即药物干预两周）处死全部大鼠，观察各组大鼠一般情况、肝组织病理学；检测各组大鼠血清肝功能水平、肝组织中羟脯氨酸（Hydroxyproline，Hyp）含量；免疫组化法检测肝组织α-平滑肌肌动蛋白（α-SMA）蛋白表达情况。结果 与正常组比较，模型组肝脏明显缩小，组织炎细胞浸润增加，胶原沉积明显增多，肝功能指标明显异常（P<0.01），提示纤维化形成。与模型组比较，黄芪甲苷可以显著改善肝脏病理，减轻肝脏胶原沉积及肝脏Hyp含量，降低血清ALT、AST、GGT水平及TBil含量，升高ALB含量，显著抑制肝组织α-SMA蛋白表达（P<0.05或P<0.01）。结论 黄芪甲苷具有显著保肝降酶抗肝纤维化形成作用，其机制可能跟抑制肝星状细胞的活化相关。 |
| 关键词: 肝纤维化 二甲基亚硝胺 黄芪甲苷 效应评价 |
| DOI：10.3969/j.issn.1674-070X.2020.01.006 |
| 投稿时间：2019-01-19 |
| 基金项目:上海市科学技术委员会专项（15DZ1900104）；国家中医药管理局第四批中医（基础）优才（2017）。 |
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| Effects of Astragaloside IV on Dimethylnitrosamine-induced Hepatic Fibrosis in Rats |
| BAI Xue,LU Lu,LIU Zhenquan,BIAN Yanqin |
| (Beijing University of Chinese Medicine, Beijing 100029, China;Beijng Jishuitan Hospital, Beijing 100035, China;Shanghai University of Traditional Chinese Medicine, Shanghai 201203, China;Shanghai Guanghua Hospital of Integrated Traditional Chinese and Western Medicine, Shanghai 200052, China) |
| Abstract: |
| Objective To investigate the effects of astragaloside IV on dimethylnitrosamine (DMN)-induced hepatic fibrosis in rats. Methods A total of 27 male Wistar rats were selected and randomly divided into a normal group, a model group and an astragaloside IV group. Rats in the model group and astragaloside IV group were induced by intraperitoneal injection of DMN for 4 weeks. From the 3rd week of modeling, the astragaloside IV group was treated with astragaloside IV while the modeling was continued. The normal group and the model group were given the same amount of distilled water. At the end of 4 weeks (2 weeks of drug intervention), rats were sacrificed and samples of each group were observed for the general situation, liver histopathology; serum liver function level and hydroxyproline (Hyp) content in liver tissue of each group of rats were detected. The expression of a-SMA protein in liver tissue was detected by immunohistochemistry. Results Compared with the normal group, the liver of the model group was significantly reduced. Tissue inflammation cell infiltration increased. The collagen deposition in the model group increased significantly. Liver function indicators were significantly abnormal(P<0.01). These suggested the formation of fibrosis. Compared with the model group, astragaloside IV can significantly improve liver pathology, alleviate liver collagen deposition and liver hydroxyproline content, reduce serum levels of ALT, AST, GGT and TBi contents, increase ALB content, significantly inhibit the expression of α-SMA protein in liver tissue (P<0.05 or P<0.01). Conclusion Astragaloside IV has significant effects of protecting liver and reducing enzymes on liver fibrosis, and the mechanism may be related to inhibiting the activation of hepatic stellate cells. |
| Key words: hepatic fibrosis dimethylnitrosamine astragaloside IV effect evaluation |
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