Erlotinib can halt adenine induced nephrotoxicity in mice through modulating ERK1/2, STAT3, p53 and apoptotic pathways

摘要: Renal fibrosis is a failed regenerative process that facilitates chronic kidney disease progression. The current study was designed to the effect of erlotinib, receptor tyrosine kinase inhibitor, on progression renal fibrosis. included four groups mice: control group; adenine group: received (0.2% w/w) daily with food for 4 weeks; erlotinib 80 mg/kg/day orally (6 ml/kg/day, 1.3% w/v suspension in normal saline 0.9%) adenine + erlotinib and concurrently. Kidney function antioxidant biomarkers were measured. expression Bcl2 p53 histopathological changes (tubular injury fibrosis) scored. tissue levels transforming growth factor-β1, p-ERK1/2 p-STAT3 Results obtained showed significant decrease (P < 0.001) serum creatinine, urea uric acid erlotinib + adenine group. Level malondialdehyde decreased significantly while reduced glutathione catalase increased (P < 0.01) by concurrent administration. Erlotinib markedly tubular TGF-β1, (P < 0.5). In addition, level Bcl-2 elevated p53-was compared alone. can attenuate development through anti-fibrotic, anti-apoptotic pathways.