The selective tyrosine kinase-inhibitor nilotinib alleviates experimentally induced cisplatin nephrotoxicity and heptotoxicity |
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| Affiliation: | 1. Pharmacology and Toxicology, College of Pharmacy, Taibah University, El-Madinah El-Munawarah, Saudi Arabia;2. Department of Clinical Pharmacology, Faculty of Medicine, Cairo University, Egypt;3. Faculty of Medicine, Taibah University, Saudi Arabia;4. Department of Histology and Cell Biology, Faculty of Medicine, Zagazig University, Egypt;5. Department of Clinical Pharmacology, Faculty of Medicine, Suez Canal University, Egypt;1. Department of Clinical Laboratory Medicine, Shanghai Tenth People’s Hospital of Tongji University, Shanghai 200072, PR China;2. Department of Central Laboratory, Shanghai Tenth People’s Hospital of Tongji University, Shanghai 200072, PR China;3. Shanghai Municipal Hospital of Traditional Chinese Medicine Affiliated to Shanghai TCM University, Shanghai 200071, PR China;1. Graduate Program in Cell and Structural Biology, Institute of Biology, State University of Campinas – UNICAMP, Campinas, Brazil;2. Department of Morphology, São Paulo State University (Unesp), Institute of Biosciences, Botucatu, Brazil;3. Graduate Program in Genetics, São Paulo State University (Unesp), Institute of Biosciences, Botucatu, Brazil;1. Center for Diagnostic Nanosystems, Marshall University, Huntington, WV 25755, USA;2. School of Pharmacy, Marshall University, Huntington, WV 25755, USA;3. Southeast University, Nanjing, Jiangsu, China;4. Huntington VA Medical Center, Huntington, WV 25704, USA;5. Department of Internal Medicine, Joan C. Edwards School of Medicine, Huntington, WV 25755, USA;1. College of Life Science and Engineering, Shenyang University, Shenyang city 110044, China;2. College of Food, Shenyang Agricultural University, Shenyang city 110866, China |
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| Abstract: | 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-κB) 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 Bcl2, increased caspase 3 activity, and NF-κB nuclear expression in both organs. Nilotinib treatment with CP restored kidney and liver oxidants/antioxidant levels also increased Bcl2 and decreased NF-κB 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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| Keywords: | Cisplatin Nilotinib Hepato-Nephrotoxicity Oxidative stress Apoptosis |
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