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瘦素是肥胖基因编码,主要由脂肪细胞合成和分泌的多肽激素,通过与其受体结合发挥抑制饮食、减少能量摄入、增加能量消耗等生物学作用。目前心肌缺血/再灌注损伤的机制尚未完全阐明,氧自由基生成、钙超载和白细胞的激活可能是其发生的主要机制。心肌缺血/再灌注损伤的保护是心血管领域研究的重点,大量研究工作证实,尽管不断地改进心肌保护方法,缺血/再灌注后的心肌细胞损伤仍无法完全避免。本文就瘦素与心肌缺血/再灌注损伤的关系予以综述。
Leptin, encoded by obesity gene, is a polypeptide hormone mainly synthesized and secreted by adipocytes. It plays a biological role in inhibiting diet, reducing energy intake and increasing energy consumption by binding to its receptors. At present, the mechanism of myocardial ischemia / reperfusion injury has not been fully elucidated. Oxygen free radical generation, calcium overload and activation of leukocytes may be the main mechanism of myocardial ischemia / reperfusion injury. Myocardial ischemia / reperfusion injury protection is the focus of cardiovascular research, a large number of studies have confirmed that, despite continuous improvement of myocardial protection methods, myocardial cell injury after ischemia / reperfusion can not be completely avoided. This article reviews the relationship between leptin and myocardial ischemia / reperfusion injury.