Infliximab ameliorates vancomycin-triggered nephrotoxicity: Biochemical, molecular, and histopathological insights.

This study investigated the pathophysiological effects of vancomycin (VCM)-induced nephrotoxicity and the potential protective role of infliximab (INF). Twenty-eight male Wistar Albino rats (200 ± 20 g) were randomly divided into four groups (n = 7): Control, INF, VCM, and VCM + INF. The Control group received physiological saline; the INF group received a single intraperitoneal (i.p.) dose of 7 mg/kg INF; the VCM group received 200 mg/kg VCM (i.p., twice daily for 7 days); and the VCM + INF group received INF 24 h prior to VCM administration. Body weight and kidney index were recorded. Serum BUN and creatinine, and renal tissue levels of MDA, SOD, and GSH were measured. Gene expression levels of Akt1, Nrf2, HO-1, Bax, Bcl-2, Caspase-3, Beclin1, Hsp27, and Hsp70 were analyzed by qRT-PCR. Histopathological evaluation was performed using hematoxylin-eosin staining, while apoptosis was assessed by immunohistochemical staining of cleaved caspase-3. VCM significantly reduced body weight, increased kidney index, and elevated BUN, creatinine, and MDA levels, while reducing SOD and GSH. INF treatment significantly reversed these effects. VCM also upregulated pro-apoptotic, autophagy, and stress response genes, while downregulating anti-apoptotic and antioxidant genes; these changes were significantly corrected by INF. Histopathological analysis showed tubular damage and inflammation in the VCM group, ameliorated by INF. Cleaved caspase-3 expression increased with VCM but was suppressed by INF. These findings indicate that infliximab provides multifaceted protection against VCM-induced kidney injury by modulating oxidative stress, apoptosis, and autophagy. This reno-protective potential of INF can be considered a novel therapeutic strategy for VCM-induced nephrotoxicity.