Infliximab abrogates adenine-induced chronic kidney disease via modulation of the MAPK/JNK/ASK signaling pathway in rats.

Chronic kidney disease (CKD) is a prominent cause of death worldwide. Infliximab is one of the anti-TNF-α; herein, we studied the effect of infliximab on adenine-induced CKD. To inspect the role of infliximab, either ameliorative or curative, on CDK induced with adenine. Thirty Wistar albino rats were separated into five groups of 6 rats' each: rats of group Ι were kept as control given saline, rats of group II were treated with infliximab (5 mg/kg, i.p.) for 5 weeks, rats of group ΙΙΙ (the diseased group) had an adenine containing diet (0.25% W/W in feed) for 5 weeks, rats of group ΙV (the ameliorative group) had an adenine-containing diet and infliximab (5 mg/kg, i.p.) for 5 weeks simultaneously, and rats of group V (the curative group) had adenine containing diet then a single dose of infliximab (5 mg/kg, i.p.) was given in the 6th week. Infliximab treatment revealed a decrease in the plasma levels of urea, creatinine, NGAL, and MDA with a substantial increase in TAC. Also, inflammatory mediators such as IL-6 and NF-κB were significantly decreased with the down-regulation of the ASK1/MAPK/JNK pathway. Caspase 3 was downregulated. Also, infliximab treatment exhibited improvement in the histological and immunohistochemical kidney changes. Through its involvement in reducing oxidative stress, inflammation, and apoptosis, infliximab has an ameliorative and curative effect on CKD induced with adenine.