Journal
ENVIRONMENTAL TOXICOLOGY AND PHARMACOLOGY
Volume 55, Issue -, Pages 60-67Publisher
ELSEVIER SCIENCE BV
DOI: 10.1016/j.etap.2017.08.008
Keywords
Cisplatin; Nilotinib; Hepato-Nephrotoxicity; Oxidative stress; Apoptosis
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This work tested the action of nilotinib, selective inhibitor of.tyrosine kinase on cisplatin (CP)-induced damage of kidney and liver in rats. Rats were assigned to 4 groups, control, nilotinib, CP, and CP plus nilotinib. Assessment of kidney and liver function, lipid peroxidation and antioxidant markers, anti-apoptotic protein Bcl2, nuclear factor- kappa B (NF-kappa B) immunoreactivity, and caspase 3 activity were done. CP-induced damage evidenced by histopathological changes, deterioration of renal and liver function, imbalance in oxidants/antioxidants markers, decreased Bc12, increased caspase 3 activity, and NF-kappa B nuclear expression in both organs. Nilotinib treatment with CP restored kidney and liver oxidants/antioxidant levels also increased Bc12 and decreased NF-kappa B immunoreactivity were evident with nilotinib treatment. In conclusions these results demonstrated a protective effect of nilotinib in experimentally induced CP kidney and liver damage that could be mediated through combating oxidative stress, reducing inflammation and anti-apoptosis in the two organs.
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