Statins exert beneficial effects in chronically damaged tissues. Angiotensin II (Ang II) participates in liver fibrogenesis by inducing oxidative stress, inflammation and transforming growth factor 1 (TGF-1) expression. We investigate whether Ator modulates Ang II-induced pathogenic effects in the liver. Male Wistar rats were infused with saline or Ang II (100 ng/Kg/min) for 4 weeks through a subcutaneous osmotic pump. Rats received either vehicle or Ator (5 mg/Kg/day) by gavage. Angiotensin II infusion resulted in infiltration of inflammatory cells (CD43 immunostaining), oxidative stress (4-hydroxynonenal), hepatic stellate cells (HSC) activation (smooth muscle -actin, -SMA) and increased intercellular adhesion molecule (ICAM-1) and interleukin-6 hepatic gene expression (quantitative PCR). These effects were markedly blunted in rats receiving Ator. The beneficial effects of Atorvastatin were confirmed in an additional model of acute liver injury (carbon tetrachloride administration). We next explored whether the beneficial effects of Ator on Ang II-induced actions are also reproduced at the cellular level. We studied HSC, a cell type with inflammatory and fibrogenic properties. Angiotensin II (10^-8M) stimulated cell proliferation, pro-inflammatory actions (nuclear factor B (NFB) activation, ICAM-1 expression and interleukin-8 secretion) as well as expression of procollagen 1(I) and TGF-1. All these effects were reduced in the presence of Ator (10^-7M). These results indicate that Ator attenuates the pathogenic events induced by Ang II in the liver both in vivo and in vitro. Therefore, statins could have beneficial effects in conditions characterized by hepatic inflammation.