Abstract
Rosiglitazone, peroxisome proliferator-activated receptor-gamma (PPAR gamma) ligand, is a clinically tested drug used in the treatment of diabetes. Several reports have proved that rosiglitazone is involved in the regulation of glucose and lipid homeostasis, proliferation, inflammation and differentiation. The current study was conducted to exemplify the effect of rosiglitazone on experimental hepatic toxicity induced by N-diethylnitrosamine (DENA). The groups of rats were dosed as follows: group I: normal control (2 mL kg(-1)), group II: rosiglitazone (40 mg kg(-1), b.w.), group III: DENA (200 mg kg(-1), b.w.), group IV: DENA + rosiglitazone (40 mg kg(-1), b.w.). All groups of animals were sacrificed after 22 weeks of treatment and appraised for biochemical changes and alteration in antioxidantmarkers along with histopathological modulation in rat liver. Rosiglitazone significantly (P < 0.001) altered the elevated levels of the above serum markers along with the inhibition of free radical formation by scavenging the hydroxyl ions. It also restored the levels of lipid hydroperoxide (LPO) and significantly (P < 0.001) modulated the levels of endogenous antioxidant enzymes in DENA mediated hepatocellular carcinoma (HCC). Biochemical estimation of different hepatic markers, antioxidant enzymes and histopathological studies of liver tissues support its anti hepatocarcinogenic role in experimental animals. In addition, in vitro cell line studies clearly indicate that rosiglitazone acts as an anticancer drug by inhibiting DNA synthesis.