The potential effect of infliximab, dimethyl fumarate (DMF), and their combination in ciprofloxacin-induced renal toxicity in male rats.

The aim of this study was to evaluate the effectiveness of infliximab and dimethyl fumarate (DMF) in reducing renal damage induced by ciprofloxacin. Forty rats were divided into five groups of eight each, with normal saline and CIP 600 mg IP administered to all animals in Groups 1 and 2 for ten days. Groups 3 and 4 were administered infliximab 7 mg/kg and DMF 30 mg/kg 24 hours before the CIP injections. Group 5 received a combination of infliximab/DMF after 24 hours of CIP. The levels of TNF-α, NF-Bp65, and IL-6 were measured, and the results showed that both infliximab and DMF had similar effects. However, the combination of infliximab and DMF had a robust anti-inflammatory and antiapoptotic impact, reducing TNF-α, NF-Bp65, IL-6, and Bcl-2 compared to the renal control group. Bcl-2 immuno-expression was lower in the ciprofloxacin group compared to the control group. DMF and infliximab had no effect on Bcl-2-positive cells, whereas infliximab increased the percentage of Bcl-2-positive cells substantially. CIP induced nephrotoxicity by increasing cytokine release and cell death signaling. Both infliximab and DMF are powerful TNF-α blockers that suppress cytokine release, preventing cell death and apoptosis caused by cytokines. Controlling inflammation and apoptosis can prevent nephrotoxicity.