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Comparison of murine cirrhosis models induced by hepatotoxin administration and common bile duct ligation

World Journal of Gastroenterology 2005年第27期11卷 4167-4172页

作者： Ming-Ling Chang Chau-Ting Yeh Pei-Yeh Chang Jeng-Chang Chen Liver Research Unit Department of Hepatogastroenterology Chang Gung Memorial HospitalTaoyuan Taiwan China Department of Surgery Chang Gung Children's Hospital Taoyuan Taiwan China

AIM： To build up the research models of hepatic fibrosis in ***： Inbred wild-type FVB/N mice were either treated with alpha-naphthyl-isothiocyanate （ANIT）, allyl alcohol （AA）,carbon tetrachloride （CCl4）, 3,5-diethoxycarbonyl-l,4-dihydrocollidine （DDC）, and silica, or subjected to common bile duct ligation （CBDL） to induce hepatic injury. Liver biopsies were performed every 4 wk to evaluate hepatic fibrosis over a period of 6 mo. Cumulative cirrhosis and survival curves were constructed by life table method and compared with Wilcoxon ***： Under the dosages used, there was neither mortality nor cirrhosis in AA and silica-treated groups. DDC and ANIT caused cirrhosis within 4-12 and 12-24 wk, *** showed significantly faster cirrhosis induction at high dosages without significant alteration of survival. The duration for cirrhosis induction by CCl4 ranged from 4 to 20 wk, mainly dependent upon the dosage. However, the increase in CCl4 dosage significantly worsened survival. Intraperitoneal CCl4 administration resulted in better survival in comparison with garage administration at high dosage, but not at medium and low dosages. After CBDL, all the mice developed liver cirrhosis within 4-8 wk and then died by the end of 26 ***： CBDL and administrations of ANIT, CCl4, and DDC ensured liver cirrhosis. CBDL required the least amount of time in cirrhosis induction, but caused shortened lives of mice. It was followed by DDC and ANIT administration with favorable survival. As for CCl4, the speed of cirrhosis induction and the mouse survival depended upon the dosages and the administration route.

关键词： common bile duct ligation Fibrosis Hepatotoxin Liver Mice

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The Therapeutic Effects of Baicalein on the Hepatopulmonary Syndrome in the Rat Model of Chronic common bile duct ligation

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Journal of Clinical and Translational Hepatology 2024年第5期12卷 496-504页

作者： Ziyang Zeng Yuhao Lei Chunyong Yang Xianfeng Wu Liang Zhang Zhiyong Yang Lin Chen Xiaobo Wang Karine Belguise Yujie Li Bin Yi Department of Anesthesiology Southwest HospitalThird Military Medical UniversityChongqingChina Department of Anesthesiology Chongqing Traditional Chinese Medicine HospitalChongqingChina MCD Center de Biologie IntégrativeUniversitéde ToulouseCNRSUPSToulouseFrance

Background and Aims:Hepatopulmonary syndrome(HPS)is characterized by arterial oxygenation defects due to pulmonary vascular dilation in liver *** date,liver transplantation remains the only effective treatment for *** study aimed to explore the preventative role of baicalein in HPS ***:Sixty male rats were randomly assigned to three groups:sham,common bile duct ligation(CBDL),and baicalein,receiving intraperitoneal injections of baicalein(40 mg·kg^(-1)·d^(-1),diluted in saline)for 21 *** rate,liver and kidney function,and bile acid metabolism levels were *** and lung angiogenesis and hepatic glycogen staining were assessed,and the expression of relevant proteins was evaluated by ***:Baicalein improved survival rates and hypoxemia in rats post-CBDL,reducing angiogenic protein levels and enhancing glucose *** to the untreated group,baicalein suppressed the expression of vascular endothelial growth factor,placental growth factors,matrix metalloprotease 9 and C-X-C motif chemokine 2,and it increased the expression of glycemic regulatory proteins,including dipeptidyl peptidase-4,sirtuin 1,peroxisome proliferatoractivated receptor gamma co-activator 1α,and 6-phosphofructo-2-kinase/fructose-2,6-biphosphatase ***:Baicalein significantly improves hepatic function and hypoxia in HPS rats by attenuating pathological angiogenesis in the liver and lungs,showing promise as a treatment for HPS.

关键词： Baicalein Hepatopulmonary syndrome common bile duct ligation Angiogenesis Glucose metabolism Liver fibrosis Glycolysis

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