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Hepatoprotective effect of the tyrosine kinase inhibitor nilotinib against cyclosporine‐A induced liver injury in rats through blocking the Bax/Cytochrome C /caspase‐3 apoptotic signaling pathway by Marwa S. Serrya; Manar A. Nader; Marwa E. Abdelmageed is a Biochemistry, Genetics and Molecular Biology article available to read on EtoBox.

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## Abstract Cyclosporine‐A (CsA) is a powerful immunosuppressive agent and hepatotoxicity results from CsA treatment. This study aimed to elucidate the effectiveness of tyrosine kinase inhibitor nilotinib against CsA‐induced hepatotoxicity and the underlying molecular mechanisms. Male Sprague‐Dawley rats were allocated into four groups and received drugs for 28 days as follows: Control group: received vehicle, Nilotinib group: received nilotinib (20 mg/kg orally), CsA group: received CsA by subcutaneous injection (20 mg/kg daily), CsA‐nilotinib: received nilotinib and CsA. Serum lactate dehydrogenase (LDH), liver function biomarkers, hepatic levels of oxidative stress biomarkers, nuclear factor erythroid‐2 like‐2 (Nrf2), total antioxidant capacity (TAC), interleukin‐2 (IL‐2), IL‐1β, IL‐6, and cytochrome‐C were assessed. Additionally, the protein levels and mRNA expression of Bcl2 associated X protein (Bax), caspase‐3, nuclear factor‐κB (NF‐κB), hemoxygenase‐1 (HO‐1) were measured. Moreover, liver tissues were assessed histopathologically using hematoxylin–eosin and Masson trichrome stain. Nilotinib treatment decreased serum LDH, alanine aminotransferase, aspartate aminotransferase,

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Author

Marwa S. Serrya; Manar A. Nader; Marwa E. Abdelmageed

Publisher

Wiley

Published

2021

Language

EN

Field

Biochemistry, Genetics and Molecular Biology (Life Sciences)