الفهرس | Only 14 pages are availabe for public view |
Abstract Liver fibrosis pathogenesis is complicated and varies between the different types of hepatic damage, Usually after an acute hepatic injury, this process relates to an inflammatory response and deposition of ECM when the injury continues, ultimately the regenerative response fails and the hepatocytes are substituted by abundant ECM rich in collagen, fibronectin, and elastin, liver injury produced by CCl4 depends on its metabolism to the highly reactive trichloromethyl (CCl3) radical which initiates lipid peroxidation. This leads to CCl4 hepatotoxicity by starting lipid peroxidation in membranes , Levels of some important biochemical parameters in serum are used as diagnostic markers of hepatic injury. One of the most sensitive and dramatic indicators of hepatocyte injury is the release of intracellular enzymes, such as transaminases and serum alkaline phosphatase in the circulation after CCl4 administration. The elevated activities of these enzymes are indicative of cellular leakage and loss of the functional integrity of the cell membranes in liver which is always associated with hepatonecrosis ,In this study we investigate the effect of sorafenib only and sorafenib combined with taurine or sorafenib combined with tiopronine in liver fibrosis. |