Nephrotoxicity is defined as rapid deterioration in kidney functions that arises from direct exposure to a drug or its metabolite. Methotrexate is an anti-metabolite used in low doses for autoimmune and inflammatory disorders and high doses for different malignancies. Pyridoxine is the usual form of vitamin B6 included in pharmaceutical products. This study is designed to examine the effect of pyridoxine in two different doses, each co-administered with methotrexate at 20 mg/kg made renal toxicity in rats through the involvement of Nrf2/HO-1 molecular mechanism in this respect. The animals used in this research were allocated to four distinct groups (each group with 10 rats) of both sexes; as control, MTX, pyridoxine 33 mg/kg and MTX, Pyridoxine 100 mg/kg, and MTX. Serum creatinine, neutrophil gelatinase-associated lipocalin (NGAL), and NrF2/HO-1 signaling pathway were determined. Administration of Pyridoxine (33 mg/kg intraperitoneally) in combination with MTX showed no significant differences (p >0.05) as compared to the MTX group. At the same time, administration of pyridoxine (100 mg/kg intraperitoneally) in combination with methotrexate showed a significant reduction in serum activities of both neutrophil gelatinase associated lipocalin (NGAL) and creatinine (p is less than 0.05) and significant upregulation in Nrf2/HO-1 signaling pathway each compared to corresponding levels in MTX-only group. In conclusion, this study demonstrated that when pyridoxine (100 mg/kg IP) was administered in combination with methotrexate, the renal toxicity was reduced as a result.
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