Hepatic fibrosis is a wound healing response in which damaged regions are encapsulated by extra cellular matrix, or scar. The composition of the hepatic scar is similar regardless the underlying cause. Hepatic fibrosis always follows chronic injury but not self-limited acute insult unless chronic injury follows. It starts in regions where injury is most severe. Hepatic stellate cells play an important role in the pathogenesis of liver fibrosis, as they constitute the major source of excess collagen in liver fibrosis. It has been reveled that AT-II induced contraction and proliferation of hepatic stellate cells (HSCs). AT-II also increased the transforming growth factor β1 (TGF β1) and collagen-I gene expression in the fibroblasts in vitro. These biological actions were mediated predominantly through AT1 receptors. Accordingly, AT-II and AT1 receptor interaction seems to have pivotal role in liver fibrosis development In the present study, examination of the effect of inhibiting RAS, especially angiotensin II (AT-II) and angiotensin-receptor type 1 (AT1-R) interaction, on liver fibrosis induced by administration of pig serum in male albino rats was studied. The clinically available compounds used were perindopril (an ACE inhibitor) and candesartan (AT1-R blocker) at therapeutic concentrations. We also used the hepatoprotective drug “silymarin” for comparing the hepatoprotective effects of these agents, if any, to this standard drug. Moreover, studying the effect of combined use of these drugs (perindopril and candesartan) to silymarin to explore any possible interaction on the same hepatic fibrosis animal model.