Influence of ursodeoxycholic acid on the therapeutic effects of low-calorie diet in obesity and hyperlipidemia rats with steatohepatitis / 中华肝脏病杂志

<p><b>OBJECTIVE</b>To explore the influence of ursodeoxycholic acid on the therapeutic effects of low-calorie diet in steatohepatitis with obesity and hyperlipidemia.</p><p><b>METHODS</b>Thirty-five Sprague-Dawley rats fed with high-fat diet for 10 weeks were randomly allocated into 3 groups, and continued to experiment for 2 weeks. The animals in model group (n = 10) were still fed with high-fat diet; low-calorie diet group (n = 10) with common diet but only one third of the amount of normal demand; ursodeoxycholic acid group (n = 15) with low-calorie diet and ursodeoxycholic acid (15 mg/kg.d(-1)); and another 9 rats with common diet for 12 weeks as normal group.</p><p><b>RESULTS</b>Compared with normal group, such indexes as body weight, liver weight, and the level of serum lipids and aminotransferase were all increased significantly in model group. Furthermore, all rats in model group developed steatohepatitis. On the other hand, such indexes as body weight and the degree of steatosis in rats of low-calorie diet group were decreased sharply compared with those in model group, but neither disorders of serum lipid nor the degree of hepatic inflammation and necrosis in low-calorie diet group were improved obviously. Disorders of serum lipid, aspartate aminotransferase, hepatic inflammation and necrosis in ursodeoxycholic acid group were ameliorated to some extent.</p><p><b>CONCLUSIONS</b>Ursodeoxycholic acid might help to improve the therapeutic effects of low-calorie diet on steatohepatitis with obesity and hyperlipidemia.</p>

Dynamic expression of tenascin in rat liver during liver fibrogenesis induced by CCl(4) / 中华肝脏病杂志

<p><b>OBJECTIVE</b>To study the expression of tenascin in normal and fibrotic rat liver.</p><p><b>METHODS</b>Liver fibrosis induced in rat with CCl(4) were divided into three stages: the stage of hepatic injury (4 weeks), early stage of hepatic fibrosis (8 weeks) and later stage of hepatic fibrosis (12 weeks). Tenascin expression in liver tissue was observed by immunohistochemical method and in situ hybridization using digoxigenin-labelled DNA probe.</p><p><b>RESULTS</b>In normal rat liver there was a weak staining for tenascin. In both liver injury stage and early stage of hepatic fibrosis, both mRNA signal and immunostaining for tenascin were significantly increased as compared to that in normal liver. In later stage of hepatic fibrosis, mRNA signal and immunostaining for tenascin were decreased compared with that in early stage of hepatic fibrosis. The cellular source of tenascin in liver mainly restricted in mesenchymal cells.</p><p><b>CONCLUSIONS</b>Tenascin is a component of the extracellular matrix of liver tissue. Plays a role in early matrix organization during liver fibrogenesis.</p>