الفهرس 
INTRODUCTIONOnly 14 pages are availabe for public view
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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.