Platelet-activating factor (PAF), a

血小板活化因子（PAF）是一种生物活性磷脂，在细胞膜结构的完整性中起着重要作用，并参与了心肌缺血/再灌注（IR）损伤的发病机制。在这项研究中，我们测试了BN 52021（银杏内酯B）阻断PAF受体可以预防IR诱导的心肌膜磷脂降解和心脏功能恶化的假设。对大鼠心脏进行原位缺血5分钟，然后再灌注10分钟。监测缺血和再灌注期间的心脏性能，并分析膜磷脂的量。与假手术大鼠心脏相比，缺血再灌注大鼠心脏中的心肌总磷脂，磷脂酰胆碱和磷脂酰乙醇胺显着降低。膜磷脂的降解伴随着心脏功能的恶化和血清乳酸脱氢酶（LDH）活性的增加。BN 52021（15 mg / kg），在冠状动脉左前降支闭塞前10分钟静脉输注，减少了IR相关的心肌磷脂降解，血清LDH活性，并伴有心脏功能改善。此外，我们证明了培养的缺氧心肌细胞中PAF的产生增加，而BN 52021减少了细胞损伤。这些结果表明PAF拮抗剂BN 52021对IR引起的心肌功能障碍和膜磷脂降解具有保护作用。

血小板激活因子（PAF）是一种生物活性磷脂，在细胞膜结构的完整性中起着重要作用，并参与心肌缺血/再灌注（IR）损伤的发病机制。在这项研究中，我们检验了由BN 52021（金基利德B）阻断PAF受体的假说，可以防止心肌膜磷脂的红外降解和心脏功能恶化。原地鼠心受到5分钟缺血，随后10分钟再灌注。监测缺血和再灌注期间的心脏表现，分析膜磷脂量。与假操作大鼠心脏相比，缺血-再灌注大鼠心脏的心肌总磷脂、磷脂酰胆碱和磷脂乙酰胺显著降低。膜磷脂的降解伴随着心脏功能的恶化和血清乳酸脱氢酶（LDH）活性的增加。BN 52021 （15 mg/kg），在左前冠状动脉闭塞前 10 分钟静脉输液，减少心肌磷脂的 IR 相关降解，血清 LDH 的活性，并伴随心脏功能的改善。此外，我们证明PAF的产量增加，BN 52021减少了培养性厌氧体细胞损伤。这些结果表明，PAF拮抗剂BN 52021对IR诱导的心肌功能障碍和膜磷脂降解具有保护作用。

Platelet-activating factor (PAF), a bioactive phospholipid, plays an important role in the integrity of the cellular membrane structure, and is involved in the pathogenesis of myocardial ischemia/reperfusion (IR) injuries. In this study, we tested the hypothesis that blockage of PAF receptor by BN 52021 (Ginkgolide B) can prevent IR-induced degradation of the myocardial membrane phospholipid, and deterioration of the cardiac function. Rat hearts in situ were subjected to 5 min ischemia and followed by 10 min reperfusion. Cardiac performances during periods of ischemia and reperfusion were monitored, and the amount of membrane phospholipids was analyzed. Myocardial total phospholipids, phosphatidylcholine, and phosphatidylethanolamine were decreased significantly in ischemia-reperfusion rat hearts compared with those of sham-operated rat hearts. Degradation of the membrane phospholipid was accompanied by the deterioration of cardiac functions and increase in serum lactate dehydrogenase (LDH) activity. BN 52021 (15 mg/kg), given by intravenous infusion 10 min prior to the left anterior descending coronary artery occlusion, reduced IR-related degradation of the myocardial phospholipids, the activity of serum LDH, and was concomitant with improvement of cardiac function. Furthermore, we demonstrated that the production of PAF was increased and BN 52021 decreased cellular damage in cultured anoxic cardiomyocytes. These results indicated that PAF antagonist BN 52021 has a protective effect against IR-induced myocardial dysfunction and degradation of the membrane phospholipids.<br>