الفهرس 
IntroductionOnly 14 pages are availabe for public view
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Abstract
The way cells respond to various stresses can either produce a signal of repair or cell death according to the type of stress. Since there are similarities between cell death/repair /regeneration during tissue damage and cancerous cells, hence there may be a new role of this tyrosine kinase inhibitors in changing body response to drug target organ toxicities.
In this context, the current thesis provides a way for investigating these new roles of tyrosine kinase pathways during adenine induced kidney injury using EGF inhibitor erlotinib and VEGF inhibitor sunitinib. This study proved the protective capability of receptor tyrosine kinase inhibitors sunitinib and erlotinib in protection against adenine induced nephrotoxicity possibly through antioxidant, and antifibrotic mechanisms. They also interfere with Erk1/2, STAT3 and TGF-β1 pathways. Finally, they may have an anti-apoptotic effect limiting renal tissue damage and dysfunction. Erlotinib showed better effect in decreasing fibrosis score and regaining oxidative stress-antioxidant balance.