Corresponding Author Antinecroinflammatory Effects of Atorvastatin Against Carbon Tetra Chloride-induced Hepatotoxicity in Rats Antinecroinflammatory Effects of Atorvastatin Against Carbon Tetra Chloride-induced Hepatotoxicity in Rats

Abstract

ABSTRACT Atorvastatin is widely used in the treatment of hepatic disease. The aim of present study is to determine the necroinflammatory activity of atorvastatin against CCl 4 -induced hepatotoxicity in rats. 30 Adult Wistar male albino rats were collected and these rats divided randomly into 5 groups. Group I was as Control group and received intraperitoneal injection of saline (1mg.kg -1 ), Group II received CCl (1 mg/kg, s.c), Group III received Atorvastatin (5 mg/kg, p.o) +CCl (1 mg/kg, i.p), Group IV received Atorvastatin (10 mg/kg, p.o) +CCl (1 mg/kg, i.p) and Group V received Atorvastatin (15 mg/kg, p.o) +CCl (1 mg/kg, i.p) for 28 consecutive day. At the 28 day blood samples from all rats of every group were collected and levels of SGPT, SGOT, ALP and Bilirubin by standard kits were assayed. The liver tissues were taken for histopathological examination. From histopathological study in group I no abnormal changes were observed and in group II, III and IV different abnormal changes with different degrees consist of fatty change, lymphocytic infiltration, necrosis, congestion and hemorrhage were distinguished.in end for Group V no fatty change were observed and was similar to normal hepatocyte. The animals treated with CCl 4 exhibited a significant (P<0.001) rise in SGOT, SGPT, ALP and bilirubin levels when compared to the control group. The results of this study clearly demonstrated that the atorvastatin exhibited potent hepatoprotective activity against CCl 4 -induced hepatic damage in rats. This may be due to their antioxidant and free radical scavenging properties. In this study, an increase in the activities of SGPT, SGOT, ALP and bilirubin in serum evidenced the CCl4 -induced hepatocellular damage because these are cytoplasmic in location and are released into the circulation after cellular damage