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肝胆相照论坛 论坛 学术讨论& HBV English 茵陈蒿汤通过调节胆汁酸代谢和TGF-β/ Smad / ERK信号通 ...
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发表于 2018-10-24 13:49 |只看该作者 |倒序浏览 |打印
Yinchenhao Decoction Alleviates Liver Fibrosis by Regulating Bile Acid Metabolism and TGF-β/Smad/ERK Signalling Pathway

    Fei-Fei Cai, Rong Wu, Ya-Nan Song, Ai-Zhen Xiong, Xiao-Le Chen, Meng-Die Yang, Li Yang, Yuanjia Hu, Ming-Yu Sun & Shi-Bing Su

Scientific Reports volume 8, Article number: 15367 (2018) | Download Citation
Abstract

Yinchenhao decoction (YCHD), comprising Yinchenhao (Artemisiae Scopariae Herba), Zhizi (Gardeniae Fructus) and Dahuang (Radix Rhei et Rhizoma), is widely used for treating various diseases. We aimed to investigate the bile acid metabolic mechanism of YCHD in dimethylnitrosamine (DMN)-induced liver fibrosis model. Rats received DMN (10 mg/kg, intraperitoneally) for four successive weeks for liver fibrosis induction and were treated with YCHD for the last 2 weeks. Histopathological analysis showed that YCHD prevented DMN-induced histopathological changes in liver tissues. Serum liver function in YCHD group improved. Ultraperformance liquid chromatography-mass spectrometry analysis showed that YCHD significantly restored both free and conjugated bile acid levels increased by DMN, to normal levels. RT-qPCR results showed that YCHD treatment upregulated the expression of genes related to bile acid synthesis, reabsorption, and excretion. Western blotting analysis showed that YCHD downregulated α-SMA, TGF-β1, p-Smad3, and p-ERK1/2 expression in chenodeoxycholic acid (CDCA)-activated hepatic stellate cells (HSCs). The viability of CDCA-activated HSCs significantly increased after treatment with YCHD and PD98059 (an ERK inhibitor) compared to YCHD treatment alone. Our findings suggest that YCHD alleviated DMN-induced liver fibrosis by regulating enzymes responsible for bile acid metabolism. Additionally, it inhibits CDCA-induced HSC proliferation and activation via TGF-β1/Smad/ERK signalling pathway.

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62111 元 
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30437 
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2009-10-5 
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2022-12-28 

才高八斗

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发表于 2018-10-24 13:50 |只看该作者
茵陈蒿汤通过调节胆汁酸代谢和TGF-β/ Smad / ERK信号通路来缓解肝纤维化

    蔡飞飞,吴荣,宋亚南,熊爱珍,陈晓乐,杨梦蝶,李阳,胡元嘉,孙明宇,苏世兵

Scientific Reportsvolume 8,货号:15367(2018)|下载引文
抽象

茵陈蒿汤(YCHD),包括茵陈蒿(Artemisiae Scopariae Herba),栀子(栀子)和大黄(Radix Rhei et Rhizoma),广泛用于治疗各种疾病。我们旨在研究YCHD在二甲基亚硝胺(DMN)诱导的肝纤维化模型中的胆汁酸代谢机制。大鼠接受DMN(10mg / kg,腹膜内)连续四周用于肝纤维化诱导,并且在最后2周用YCHD治疗。组织病理学分析显示YCHD阻止DMN诱导的肝组织组织病理学变化。 YCHD组血清肝功能改善。超高效液相色谱 - 质谱分析表明,YCHD显着恢复DMN增加的游离和结合胆汁酸水平至正常水平。 RT-qPCR结果显示,YCHD处理上调了与胆汁酸合成,再吸收和排泄相关的基因的表达。 Western blotting分析显示,YCHD可下调鹅去氧胆酸(CDCA)激活的肝星状细胞(HSC)中的α-SMA,TGF-β1,p-Smad3和p-ERK1 / 2的表达。与单独的YCHD治疗相比,用YCHD和PD98059(ERK抑制剂)治疗后CDCA活化的HSC的活力显着增加。我们的研究结果表明,YCHD通过调节负责胆汁酸代谢的酶来减轻DMN诱导的肝纤维化。另外,它通过TGF-β1/ Smad / ERK信号传导途径抑制CDCA诱导的HSC增殖和活化。

Rank: 8Rank: 8

现金
62111 元 
精华
26 
帖子
30437 
注册时间
2009-10-5 
最后登录
2022-12-28 

才高八斗

3
发表于 2018-10-24 13:50 |只看该作者
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