Hepatoprotective effects of Mimic of Manganese superoxide dismutase against carbon tetrachloride-induced hepatic injury

• We investigated the protective effects of MnSODm against CCl4-induced hepatic injury in mice.
• MnSODm was beneficial in the prevention of CCl4-induced liver toxicity.
• MnSODm against hepatic injury possibly by reducing oxidative stress and suppressing inflammatory responses

The aim of this study was to investigate the protective effects of Mimic of Manganese superoxide dismutase (MnSODm) against carbon tetrachloride (CCl4)-induced hepatic injury in mice. Bifendate or MnSODm was intragastrically administered per day for 7 days. On the 8th day, all mice except the normal group were given 0.5% CCl4/peanut oil to induce hepatic injury model by intraperitoneal injection. Mice were sacrificed 24 h after CCl4 treatment. Compared with the CCl4 group, MnSODm significantly decreased the activities of aspartate aminotransferase (AST) and alanine aminotransferase (ALT) in the serum and increased the activities of superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) in the serum and liver. Moreover, the contents of hepatic and serum malondialdehyde (MDA) and nitric oxide (NO) with inducible nitric oxide synthase (iNOS) activities were reduced. Histological findings also confirmed the antihepatotoxic characterization. In addition, MnSODm inhibited the pro-inflammatory mediators, such as prostaglandin E2 (PGE2), cyclooxygenase-2 (COX-2), interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α). Further investigation showed that the inhibitory effect of MnSODm on the pro-inflammatory cytokines was associated with the down-regulation of nuclear factor-kappa B (NF-κB). In brief, our results show that the protective effect of MnSODm against CCl4-induced hepatic injury may rely on its ability to reduce oxidative stress and suppress inflammatory responses.