الفهرس 
INTRODUCTIONOnly 14 pages are availabe for public view
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Abstract
Diabetes consider one of the most devastating metabolic syndrome affecting around 7% of people worldwide with many serious complication as diabetic; nephropathy, retinopathy, cardiomyopathy, infertility and increase risk of limb amputation. The pathophysiological mechanism of Type 1 diabetes underlying the hyperglycemic state which potentiated several peripheral and central molecular pathways as; oxidative, inflammatory, apoptotic pathways, unfolded protein response (UPR), endoplasmic reticulum stress, downregulation of; cellular, nuclear receptors and tissues growth factors such as (VEGF, FGF, IGF).
The fore mentioned consequences affected the physiology of the different body systems reflected by many diabetic complication so the present study was designed to investigate the effect of type 1 diabetes on the different molecular pathways related to beta cells dysfunction, diabetic; male infertility and nephropathy either; peripherally and/or centrally with an attempt to introduce a new therapeutic implications of Br-MSCs to ameliorate diabetic; beta cell dysfunction, male infertility and nephropathy.
Forty five adult male SD rats were divided into three group; control, diabetic, diabetic treated with Br-MSCs double dose with 14 days interval 2weeks post validation of type1 diabetes onset. Type 1 diabetes was induced with single intraperitoneal injection of STZ 65 mg/kg. For the frist experiment the Body weight, fasting blood glucose, serum insulin level, survivability %, HOMA indices, lipid perioxidation and antioxidant activity were assayed also, qRT-PCR for pancreatic (PDX1, Ngn3, VEGF, FGF, IGF, TGFβ1, IRA, IRB, INS, PPAR-γ, TNFα, NFKβ, IL1β, IL6, IL8 , TGFβ1, MCP1, IL10, ATF3, ATF6, CHOP, JNK, BIP and XBP1, mTOR, FAS, FAS L, BAX, Caspase3, P53, P38, BCL2 and BAX/BCL2) and histopathologhical examination for pancreas were done.