| BACKGROUNDUrocortin (UCN) is a 40-amino-acid peptide related to the hypothalamic hormone corticotrophin releasing factor (CRF), the central mediator of the hypothalamic-pituitary-adrenal axis and stress response in mammals. CRF family exert their physiological effects through binding to two G protein-coupled receptors (CRFR) 1 and 2, to modulate endocrine, autonomic, and behavioral responses to stress. Urocortin was firstly found in the central nervous system. However, recent studies showed that it has much more potent effects on the cardiovascular system than CRF. It enhanced cardiac contractility, coronary blood flow, heart rates and cardiac output. Some in vitro & ex vivo investigations showed that in case of ischemia/reperfusion (I/R), atherosclerosis and hypertension, urocortin could protect cardiac cells from severe injury. Pretreatment of cardiac myocytes with urocortin could improve myocytes' condition via PI-3K, Ras, Raf-1 passway to active the mitogen-activated protein kinase (MAPK) pathway, protein kinase C and ATP sensitive K+ (PKC/KATP) channels etc. Our recent in vivo study demonstrated that urocortin could reduce cardiac damage in I/R model. Moreover, we firstly found that urocortin could inhibit the proliferation of the vascular smooth muscle cells, highly suggesting that urocortin might play a role in reversing cardiovascular remodeling and urocortin has the potent protective effects in cardiovascular system. AIM 1. The aim of this study was to investigate the effects of urocortin onoxidative stress and the mechanisms of urocortin on ischemiareperfusion (I/R) injury in vivo in the rat model. |
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