Abstract

Background: Cardiac apoptosis was found in diabetes but very limited information regarding the effects of exercise training on cardiac apoptosis in diabetes was available. The purpose of this study was to evaluate the therapeutic effects of exercise training on cardiac apoptotic pathways. METHODS: Eight Wistar rats and Streptozotocin-induced diabetic rats at 4 months of age were served as negative (Control) and positive (DM) control. Eight Streptozotocin-induced diabetic rats underwent running exercise on treatmill 1 hour daily, 5 sections per week, for 8 weeks (DM-EX). After exercise training or sedentary status, the excised hearts were measured by positive TUNEL assays and Western Blotting. RESULTS: Citrate synthase activity in skeletal muscle in DM-EX is significantly increased compared with sedentary group (Control and DM). Protein levels of mitochondria dependent pathway, including cytochrome c, activated caspase 9, and activated caspase 3 were increased in DM group compared with control. Protein levels of death receptor dependent pathway, including TNF-alpha, Fas ligand, Fas death receptors, Fas-associated death domain (FADD), activated caspase 8, and activated caspase 3 were increased in DM group compared with control. Exercise training decreased diabetes-induced cardiac TUNEL-positive apoptotic cells. Exercise training decreased protein levels of cytochrome c, activated caspase 9, activated caspase 3 (mitochondria pathway) and TNF-alpha, Fas ligand, Fas death receptors, FADD, activated caspase 8, and activated caspase 3 (Fas pathway) in DM-EX group compared with DM group. CONCLUSIONS: Exercise training suppressed diabetes-induced cardiac mitochondria and Fas receptor dependent apoptotic pathways. The findings may provide one of possible therapeutic approaches for preventing cardiac apoptosis in diabetes.

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