Motivation/problem statement: Sepsis is defined systemic inflammatory response syndrome (SIRS) after serious microbial infection. The liver is the main organ for bacterial scavenging, bacterial products inactivation, and inflammatory mediator clearance and production. Macrophages in liver can clear the endotoxin and bacteria that initiate the systemic inflammatory response. The hepatic dysfunction can be viewed as a primary dysfunction that occurs in the first hours after sepsis. Simvastatins are a class of drugs used to lower cholesterol levels by inhibiting the enzyme HMG-CoA reductase, also it has anti-inflammatory activities. We aimed to investigate effects of simvastatin on hepatic tissue in rats with Lipopolysaccharides (LPS). Methods/procedure/approach: Following the approval of the ethical commitee male Wistar albino rats were used in this study. The rats were divided into four groups as control (n=10) LPS(n=10). Simvastatin (n=10), LPS+Simvastatin groups (n=10). Sepsis was induced by administration of LPS (E.coli O127:B8; 20 mg/kg, i.p) in anesthetized rats. After 4 hours, animals were taken experiment. Simvastatin was given (20 mg/kg, p.o.) for 5 days.At the end of the 5th days animals were decapitated. Histopathologic changes in the liver sections stained with hematoxylin and eosin in all groups. Results: We seen large sinusoidal structure, degenerative lobule and cell membrane, increment of glycogen droplets and collagen in LPS and simvastatin groups in hepatic tissue sections, compared to control. In LPS+Simvastatin groups, tissue histology is as same as control’s. Also hepatic tissue has normal sinusoidal and lobule structure, and glycogen droplets. Conclusion/implications: The changes in the histologic structure of the liver were significantly affected by only treated simvastatin or LPS. Simvastatin administration in LPS treated animals improved to hepatocellular degeneration.