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Cholesterol-induced stimulation of postinflammatory liver fibrosis.

作者信息

Schwartz Y Sh, Dushkin M I, Komarova N I, Vorontsova E V, Kuznetsova I S

机构信息

Institute of Therapy, Siberian Division of the Russian Academy of Medical Sciences, Novosibirsk. Russia.

出版信息

Bull Exp Biol Med. 2008 Jun;145(6):692-5. doi: 10.1007/s10517-008-0175-6.

DOI:10.1007/s10517-008-0175-6
PMID:19110552
Abstract

We studied the effect of high-cholesterol diet and factors inhibiting 3-hydroxy-3-methylglutaryl coenzyme A reductase on the development of liver fibrosis in C57Bl/6 mice with CCl4- or zymosan-induced hepatitis. Feeding a high-cholesterol diet led to a sharp increase in collagen content in the liver tissue of animals with CCl4-induced or zymosan-induced hepatitis. Atorvastatin and calcitriol produced less pronounced fibrogenic effects. Mevalonate partially prevented the development of cholesterol-induced fibrogenesis. High-cholesterol diet led to accumulation of oxysterols, cholesterol esters, and triglycerides and increased the expression of transforming growth factor-beta1 mRNA in liver tissue. Cholesterol-induced potentiation of the fibrogenic response is probably associated with transforming growth factor-beta1 induction due to accumulation of lipids and oxysterols in the liver.

摘要

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