催产素（oxytocin, OT）是一种由下丘脑室旁核、视上核合成分泌并储存在神经垂体的生殖系统激素。文章总结了近年来国内外文献中无论是内源性OT还是外源性OT，缺血/再灌注前还是缺血/再灌注后给药，均对心脏缺血/再灌注损伤（ischemia/reperfusion injury, I/RI）具有保护作用。研究表明，OT通过增加心肌细胞对葡萄糖的吸收增强对缺血的耐受性，作用于线粒体通透性转换孔（mitochondrial permeability transition pore, mPTP）、线粒体ATP敏感性K+通道（mitochondrial adenosine triphosphate‑dependent potassium channel, mitoKATP）减轻细胞内钙超载，通过减少活性氧簇（reactive oxygen species, ROS）产生、增加抗氧化物含量等方式减轻氧化应激，抑制炎细胞聚集与炎症因子产生减轻炎症反应，促进保护性分子一氧化氮（nitric oxide, NO）和心房利钠肽（atrial natriuretic peptide, ANP）等发挥抗I/RI效应。OT作为一种“老”激素，其心脏保护的“新”角色值得进一步研究。
Oxytocin (OT) is regarded as a reproductive system hormone which is produced by the paraventricular nucleus and supraoptic nucleus of the hypothalamus and is stored at the neurohypophysis. It is reported that no matter endogenous or exogenous OT exerts cardioprotective effects against the ischemia/reperfusion injury (I/RI). Previous studies suggest that OT plays a positive role in cardiac I/RI by different manners. OT enhances cell tolerance to ischemia by increasing uptake of glucose by the cardiomyocytes. OT reduces intracellular calcium overload through mitochondrial permeability transition pore (mPTP) and mitochondrial adenosine triphosphate‑dependent potassium channel (mitoKATP). OT reduces oxidative stress by reducing the production of reactive oxygen species (ROS) and increasing the content of antioxidants. OT inhibits the aggregation of inflammatory cells and the production of inflammatory cytokines to reduce the inflammatory response. OT can also promote protective molecules such as nitric oxide (NO) and atrial natriuretic peptide (ANP) to exert anti‑I/RI effect. As an "old" hormone, its novel roles in cardioprotection deserve further exploration.
Cited
)
