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11.
泽泻化学成分的研究   总被引:11,自引:1,他引:11  
从泽泻(Alisma orientalis(Sam)Juzep)块茎中分离出12个化合物,经理化性质和波谱分析,分别鉴定为:β-谷甾醇3-O-硬脂酸酯(β-sistosterol-3-O-stearate,1),正二十三烷(tricosane,2),β-俗甾醇(β-sitosterol,5),硬脂酸(stearic acid,6)1-硬脂酸甘油酯(glyeryl 1-stearate,7),胡萝卜甙6′-O-硬脂酸酯(daucosterol-6′-O-stearate,8),泽泻醇B单醋酸酯(alisol B monoacetate,9),大黄素(emodin,10),泽泻醇C单醋酸酯(alisol C monoacetate,11),环氧泽泻烯(alismoxide,12).化合物1,2,5,6,7和10为首次由该植物中获得,化合物12首次以结晶形式获得,化合物3和4的鉴定仍在进行。  相似文献   
12.
    
Liver fibrosis is a disease caused by long‐term damage that is related to a number of factors. The current research on the treatment of liver fibrosis mainly focuses on the activation of hepatic stellate cell, in addition to protecting liver cells. byakangelicin has certain anti‐inflammatory ability, but its effect on liver fibrosis is unclear. This study aims to explore whether byakangelicin plays a role in the development of liver fibrosis and to explore its mechanism. We determined that byakangelicin has a certain ability to resist fibrosis and reduce liver cell damage in a model of carbon tetrachloride–induced liver fibrosis in mice. Thereafter, we performed further verification in vitro. The signalling pathways of two important pro‐fibrotic cytokines, transforming growth factor‐β and platelet‐derived growth factor, were studied. Results showed that byakangelicin can inhibit related pathways. According to the hepatoprotective effect of byakangelicin observed in animal experiments, we studied the effect of byakangelicin on 4‐HNE–induced hepatocyte (HepG2) apoptosis and explored its related pathways. The results showed that byakangelicin could attenuate 4‐HNE–induced hepatocyte apoptosis via inhibiting ASK‐1/JNK signalling. In conclusion, byakangelicin could improve carbon tetrachloride–induced liver fibrosis and liver injury by inhibiting hepatic stellate cell proliferation and activation and suppressing hepatocyte apoptosis.  相似文献   
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