ROLE OF DIMETHYL FUMARATE (NRF2 ACTIVATOR) IN REDUCING OF CIPROFLOXACIN-INDUCED HEPATOTOXICITY IN RATS VIA THE NRF2/HO-1 PATHWAY

Abstract

The aim: The present study aims to study the effect of DMF on ciprofloxacin-induced liver damage as assessed by liver function and liver pathology and to study this effect if it is thought to activate the Nrf2 antioxidant defense mechanism. Materials and methods: G1 (control), G2 (ciprofloxacin group), G3 and G4 (two DMF groups rats treated with DMF 50mg and 100mg), and G5 and G6 (two DMF groups rats treated with DMF 50mg and 100mg) (two ciprofloxacin Plus DMF at 50 mg and 100 mg). The tests included study of liver function, Nrf2 analysis, and anti-oxidant enzyme analysis. Results: The serum blood Nrf2, HO-1, and tissue anti-oxidant enzymes all increased after ciprofloxacin treatment. The serum levels of Nrf2 and HO-1 were higher in the ciprofloxacin plus DMF groups, but anti-oxidant enzymes were lower. DMF increased Nrf2 expression in rats when ciprofloxacin caused hepatotoxicity. Conclusions: DMF lowers experimental hepatotoxicity in vivo. This effect is thought to activate the Nrf2 antioxidant defense mechanism.