Motivation/problem statement: Sepsis, which causes deterioration of the microcirculation homeostasis, biochemical and physiological changes in the blood vessels. Sepsis leads to death of the organism as a result of organ failure. Membran proteins are alpha- and beta-spektrin, ankyrin, actin (band 5) and band-3, protein 4.1 and glycophorin A,B,C have an important roles in the maintaining in structural and functional integrity and the protection of shapement of the red blood cells. Studies shown that sepsis causes increased free radicals and lipid peroxidation of membrane proteins and erythrocyte deformability in literatures. Recent studies in patients with acute systemic inflammation were reported that simvastatin inhibits vascular hyporeactivity and reduced the development of sepsis. In this study, we aimed the effects of simvastatin on membrane proteins in lipopolysaccharide (LPS) treated with Wistar albino rats. Methods/procedure/approach : Following the approval of the ethical commitee adult rats were divided into 4 groups including control, endotoxemic, simvastatin and simvastatin plus endotoxemic. Control group; was taken %0.9 NaCl (i.p.)(n=10). Endotoxemic group; LPS (E.coli: O127:B8;20 mg/kg, i.p.) was given to occuring endotoxemia, after 4 hours, animals were taken experiment (n=10). Simvastatin group: Simvastatin was given (20 mg/kg, p.o.) for 5 days and end of the 5th days animals were decapitated (n=10). Simvastatin plus Endotoxemic group: Simvastatin was given for 5 days. At the 5th days, LPS was given and after 4 hours animals were taken experiment (n=10). At the end of the experiment, blood samples were taken into tube with EDTA and erythrocytes were separated. Erythrocyte membrane proteins were detected with Sodium dodecyl sulphate polyacrylamide gel electrophoresis (SDS-PAGE). All of samples were applicated and run to SDS-PAGE with suitable molecular weight of markers. SDS-PAGE procedures were replicated three times for each samples. RESULTS: In endotoxemic group, we shown decreased α- (280 kDa) and β-spektrin (MW: 246 kDa ), ankyrin(MW: 210 kDa), compared to control group. However we found that there were disappeared bands; actin (band 5) (MW: 43 kDa) and Band-3 (MW: 100 kDa), protein 4.1(MW: 82 kDa) and glycophorin A,B,C (MW: 30 kDa) in the endotoxemic group.There were same protein bands compositions between control and simvastatin groups. CONCLUSION/IMPLICATIONS: We found that decreased membrane proteins; alpha-spectrin, beta-spectrin, ankyrin and disappeared Band-3, Actin, Protein 4.1 Glycophorin A,B,C, proteins in the endotoxemic group. We also observed that simvastatin administration in LPS treated animals, distrupted red cell membrane proteins were found to improve in the study. It may represent a compensatory defensive mechanism supporting RBC function for living organism.