DMF Attenuates Ciprofloxacin-lnduced Nephropathy in Rats via Nrf2 Pathway

Background: The pathophysiology of ciprofloxacin-induced nephropathy (CIN) is complicated by oxidative stress. The goal of this study was to see if Dimethyl Fumarate (DMF) has any antioxidant properties in a rat model of CIN. Methods: Rats were randomly assigned to six groups (n=8): control, ciprofloxacin (ciprofloxacin-induced CIS), two DMF groups (rats treated with DMF 50mg and lOOmg), and two ciprofloxacin Plus DMF groups (n=8 group) (CDC rats treated with DMF at 50 mg and 100 mg). Renal function testing, Nrf2 analysis, and anti-oxidant enzymes analysis was all done. Results: Following ciprofloxacin therapy serum blood urea nitrogen (BUN), creatinine, and anti-oxidant enzymes all rose. In the ciprofloxacin - DMF groups, serum BUN and creatinine were lower, and anti-oxidant enzymes were higher than in the ciprofloxacin group, in CIN rats, DMF upregulated Nrf2 expression. Conclusions: In vivo, DMF reduces experimental CIN. It's thought that this impact activates the Nrf2 antioxidant defenses pathway.