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salusins是影响心血管功能的多肽,salusin-α和-β能调节内质网应激的标志分子GRP78,从而减轻血清剥夺所致的培养心肌细胞损伤.本研究探讨了salusin-α和-β能否减轻心肌缺血所致的内质网应激.在整体大鼠冠状动脉左前降支(LAD)结扎2h所致心肌缺血模型上,于结扎前15min静脉注射salusin-α或-β(5或15nmol/kg),观察到高剂量组心功能和血流动力学的显著改善,缺血性心律失常尤其是室性心动过速显著减少.salusins抑制了缺血引起的GRP78以及内质网应激相关促凋亡因子caspase-12和CHOP的高表达,改善了抑凋亡因子Bcl-2的低表达.此外,在培养的大鼠H9c2心肌细胞中,salusin-α和-β均能抑制tunicamycin所诱导的内质网应激.结果表明,salusins能抑制内质网应激以及内质网应激相关的凋亡,从而保护缺血心肌.
salusins, a polypeptide that affects cardiovascular function, salusin-α and -β can regulate the endoplasmic reticulum stress marker GRP78, thereby reducing the serum-deprivation-induced injury of cultured cardiomyocytes.In this study, salusin-α and -β Whether to reduce the endoplasmic reticulum stress caused by myocardial ischemia.Under the myocardial ischemia model induced by left anterior descending coronary artery (LAD) ligature for 2h in rats, the salusin-α or -β (5 Or 15 nmol / kg), significant improvements in cardiac function and hemodynamics were observed in the high-dose group, with significant decreases in ischemic arrhythmias, particularly ventricular tachycardia. Salusins inhibited ischemia-induced GRP78 and endoplasmic reticulum In the cultured rat H9c2 cardiomyocytes, both salusin-α and -β inhibited tunicamycin Induced endoplasmic reticulum stress.The results show that salusins can inhibit endoplasmic reticulum stress and endoplasmic reticulum stress-related apoptosis, thereby protecting the ischemic myocardium.