obeticholic-acid and artenimol

Portal hypertension is a frequent pathological symptom occurring especially in hepatic fibrosis and cirrhosis. Current paradigms indicate that inhibition of hepatic stellate cell (HSC) activation and contraction is anticipated to be an attractive therapeutic strategy, because activated HSC dominantly facilitates an increase in intrahepatic vein pressure through secreting extracellular matrix and contracting. Our previous in vitro study indicated that dihydroartemisinin (DHA) inhibited contractility of cultured HSC by activating intracellular farnesoid X receptor (FXR). However, the effect of DHA on fibrosis-related portal hypertension still requires clarification. In this study, gain- and loss-of-function models of FXR in HSC were established to investigate the mechanisms underlying DHA protection against chronic CCl

Topics: Animals; Artemisinins; Carbon Tetrachloride; Cell Death; Chenodeoxycholic Acid; Gene Expression; Hepatic Stellate Cells; Hepatocytes; Humans; Hypertension, Portal; Liver; Liver Cirrhosis; Male; Mice; Mice, Inbred ICR; Mice, Transgenic; Portal Vein; Pregnenediones; Protective Agents; Rats; Rats, Sprague-Dawley; Receptors, Cytoplasmic and Nuclear