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首页> 外文期刊>The Korean Journal of Physiology & Pharmacology >Kinetic Changes of COX-2 Expression during Reperfusion Period after Ischemic Preconditioning Play a Role in Protection Against Ischemic Damage in Rat Brain
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Kinetic Changes of COX-2 Expression during Reperfusion Period after Ischemic Preconditioning Play a Role in Protection Against Ischemic Damage in Rat Brain

机译：缺血预处理后再灌注期间COX-2表达的动力学变化对大鼠脑缺血损伤的保护作用

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摘要

A brief ischemic insult induces significant protection against subsequent massive ischemic events. The molecular mechanisms known as preconditioning (PC)-induced ischemic tolerance are not completely understood. We investigated whether kinetic changes of cyclooxygenase (COX)-2 during reperfusion time-periods after PC were related to ischemic tolerance. Rats were given PC by occlusion of middle cerebral artery (MCAO) for 10 min and sacrificed after the indicated time-periods of reperfusion (1, 2, 4, 8, 12, 18 or 24 h). In PC-treated rats, focal ischemia was induced by occlusion of MCA for 24 h and brain infarct volume was then studied to determine whether different reperfusion time influenced the damage. We report that the most significant protection against focal ischemia was obtained in rats with 8 h reperfusion after PC. Administration of indomethacin (10 mg/kg, oral) or rofecoxib (5 mg/kg, oral) 48 h prior to PC counteracted the effect of PC. Immunohistochemical analysis showed that COX-2 and HO-1 protein were induced in PC-treated rat brain, which was significantly inhibited by rofecoxib. Taken together, we concluded that the kinetic changes of COX-2 expression during the reperfusion period after PC might be partly responsible for ischemic tolerance.
机译：短暂的缺血性损伤可对随后的大规模缺血性事件产生明显的保护作用。尚未完全了解称为预处理（PC）引起的缺血耐受的分子机制。我们调查了PC后再灌注期间环氧合酶（COX）-2的动力学变化是否与缺血耐受性相关。通过阻塞大脑中动脉（MCAO）10分钟给大鼠PC，在指定的再灌注时间（1、2、4、8、12、18或24 h）后处死大鼠。在PC处理的大鼠中，MCA闭塞24 h诱发局灶性缺血，然后研究脑梗塞体积，以确定不同的再灌注时间是否影响损伤。我们报告说，在PC后8 h再灌注的大鼠中获得了针对局部缺血的最显着保护作用。 PC前48小时给予消炎痛（10 mg / kg，口服）或罗非考昔（5 mg / kg，口服）可抵消PC的作用。免疫组织化学分析表明，PC处理的大鼠大脑中诱导了COX-2和HO-1蛋白，而罗非考昔显着抑制了该蛋白。两者合计，我们得出结论，PC后再灌注期间COX-2表达的动力学变化可能是局部缺血耐受的部分原因。

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