Anti-apoptotic and antioxidant effect of leptin on CCl4-induced acute liver injury in rats

The aim of this study is to investigate the effect of leptin in rats on carbon tetrachloride (CCl4) induced acute liver damage using immunohistochemical methods for apoptosis and biochemical parameters. In this experimental study, 18 Spraque-Dawley rats were divided into three groups viz; control, CCl4 and CCl4+leptin treatment. 0.8 ml/kg olive oil was administered intraperitoneally (i.p.) to the control group and 0.8 ml/kg CCl4 (1:1 dissolved in olive oil) was administered i.p. to the CCl4 and CCl4+leptin treatment groups, respectively. After 6 h of administrating CCl4, CCl4+leptin treatment group was given i.p. leptin (10 mu g/kg). Twenty-four hours after administrating CCl4 all of the groups were euthanized. Biochemical assessments were performed using serum aspartate aminotransferase (AST), alanine aminotransferase (ALT), alkaline phosphatase (ALP), plasma tumor necrosis factor alpha (TNF-alpha) levels and tissue malondialdehyde (MDA), and TNF-alpha levels. Histological assessments were then performed using Hematoxylin&Eosin (H&E) staining in light microscope and apoptosis assessment using Terminal Transferase dUTP Nick End Labeling (TUNEL)-staining. Serum AST, ALT, ALP and plasma TNF-alpha levels, tissue MDA and TNF-alpha levels had all increased in CCl4 group, but were found to be significantly decreased in CCl4+leptin treatment group. Moreover, TUNEL-positive cell counts in liver had significantly increased in CCl4 group, but decreased in CCl4+leptin treatment group (P < 0.05). The results of our study the biochemical, histological and TUNEL-staining showed that leptin has treatment effects on liver CCl4 induced injury. It plays a role as a potent free radical scavenger, a powerful antioxidant and it also has anti-apoptotic effects.