| 引用本文: | 戴鸿志,安祯祥,黄丹,唐东昕,何远利.黄芪甲苷对肝纤维化模型大鼠的改善作用机制研究[J].中国现代应用药学,2022,39(10):1268-1274. |
| DAI Hong-zhi,AN Zhen-xiang,HUANG Dan,TANG Dong-xin,HE Yuan-li.Study on Mechanism of Improvement Effects of Astragaloside IV on Hepatic Fibrosis Model Rats[J].Chin J Mod Appl Pharm(中国现代应用药学),2022,39(10):1268-1274. |
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| 黄芪甲苷对肝纤维化模型大鼠的改善作用机制研究 |
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戴鸿志1, 安祯祥2, 黄丹2, 唐东昕2, 何远利2
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1.贵州中医药大学研究生院, 贵阳 550001;2.贵州中医药大学第一附属医院, 贵阳 550001
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| 摘要: |
| 目的 观察黄芪甲苷对CCl4诱导的肝纤维化模型大鼠的改善作用及可能机制。方法 将SD大鼠随机分为正常组、模型组、水飞蓟宾组(30 mg·kg–1)、黄芪甲苷组(14 mg·kg–1)。采用50% CCl4橄榄油溶液(1.5 mL·kg–1)腹腔注射建立肝纤维化模型,每周2次,持续8周。然后各组大鼠按照每天10 mL·kg–1灌胃相应药物,共4周。检测大鼠血清中丙氨酸氨基转移酶(ALT)、天门冬氨酸氨基转移酶(AST)含量;计算肝脏指数;苏木素-伊红(HE)及Masson染色观察肝组织病理变化;Western blotting检测转化生长因子(TGF-β1)、上皮间质转化标志物E-钙黏蛋白(E-cadherin)、N-钙黏蛋白(N-cadherin)和α-平滑肌动蛋白(α-SMA)的蛋白表达水平;实时荧光定量PCR检测TGF-β1和E-cadherin的mRNA表达水平。结果 与正常组相比,模型组大鼠肝脏指数显著升高(P<0.01),血清中ALT、AST含量明显上升(P<0.01),胶原容积分数明显增加(P<0.01),肝组织内E-cadherin蛋白表达明显下降(P<0.01),α-SMA、N-cadherin蛋白表达明显升高(P<0.01),TGF-β1 mRNA及蛋白表达水平明显上升(P<0.05或P<0.01)。与模型组比较,黄芪甲苷组肝脏指数大幅下降(P<0.01),血清中ALT和AST含量明显降低(P<0.01),胶原容积分数明显下降(P<0.01),肝组织内E-cadherin蛋白表达上调(P<0.05),α-SMA、N-cadherin蛋白表达显著下调(P<0.01),TGF-β1蛋白和mRNA表达下降(P<0.01或P<0.05)。结论 黄芪甲苷对CCl4诱导肝纤维化模型大鼠具有改善作用,其机制可能与下调N-cadherin、α-SMA、TGF-β1蛋白表达,上调E-cadherin蛋白表达有关。 |
| 关键词: 黄芪甲苷 肝纤维化 上皮间质转化 E-钙黏蛋白 N-钙黏蛋白 α-平滑肌动蛋白 转化生长因子 |
| DOI：10.13748/j.cnki.issn1007-7693.2022.10.002 |
| 分类号:R285.5 |
| 基金项目:国家自然科学基金项目(82160893,81760865,81460726);贵州省科技计划项目(黔科合LH字[2017]7141号);国家中医药管理局第五批全国中医临床优秀人才研修项目(国中医药人教函[2022]1号) |
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| Study on Mechanism of Improvement Effects of Astragaloside IV on Hepatic Fibrosis Model Rats |
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DAI Hong-zhi1, AN Zhen-xiang2, HUANG Dan2, TANG Dong-xin2, HE Yuan-li2
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1.Graduate School of Guizhou University of Traditional Chinese Medicine, Guiyang 550001, China;2.The First Affiliated Hospital of Guizhou University of Traditional Chinese Medicine, Guiyang 550001, China
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| Abstract: |
| OBJECTIVE To observe the improvement effect of astragaloside IV on CCl4-induced hepatic fibrosis model rats and its possible mechanism.METHODS SD rats were randomly divided into normal group, model group, silibinin group(30 mg·kg-1), and astragaloside IV group(14 mg·kg-1). The hepatic fibrosis model was established by intraperitoneal injection of 50% CCl4 olive oil solution(1.5 mL·kg-1) twice a week for 8 weeks. Then rats in each group were given the corresponding drugs by intragastric administration of 10 mL·kg-1 per day for 4 weeks. Detected the content of alanine aminotransferase(ALT) and aspartate aminotransferase(AST) in rat serum. Calculated the liver index. Hematoxylin-eosin(HE)and Masson staining were used to observe the pathological changes of liver tissue. Western blotting were used to detect the protein expression level of transforming growth factor(TGF-β1), epithelial-mesenchymal transition(EMT) markers E-cadherin,N-cadherin and α-smooth actin(α-SMA). Real-time PCR were used to detected the mRNA expression levels of TGF-β1 and E-cadherin.RESULTS Compared with the normal group, the liver index of rats in the model group was significantly increased(P<0.01), the contents of ALT and AST in the serum were significantly increased(P<0.01), the collagen volume fraction was significantly increased(P<0.01), and TGF-β1 mRNA in the liver tissue and protein expression levels increased(P<0.05 or P<0.01), E-cadherin protein expression was significantly decreased(P<0.01), α-SMA, N-cadherin protein expression was significantly increased(P<0.01). Compared with the model group, the liver index in the astragaloside IV group significantly decreased(P<0.01), the serum ALT and AST content was significantly decreased(P<0.01), the collagen volume fraction was significantly decreased(P<0.01), and E-cadherin in the liver tissue protein expression was up-regulated(P<0.05), α-SMA,N-cadherin protein expression was significantly down-regulated(P<0.01), TGF-β1 protein and mRNA expression decreased(P<0.01 or P<0.05).CONCLUSION Astragaloside IV has an ameliorating effect on CCl4-induced hepatic fibrosis model rats, and its mechanism may be related to down-regulation of N-cadherin, α-SMA, TGF-β1 protein expression and up-regulation of E-cadherin protein expression. |
| Key words: astragaloside IV hepatic fibrosis epithelial-mesenchymal transition E-cadherin N-cadherin α-SMA TGF-β1 |
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