关键词: 核转录因子-кB, 七氟烷, 预处理, 心肌缺血再灌注损伤

Abstract: Objective To investigate the protective effects of NF-кB P65 active expression during sevoflurane preconditioning on rat myocardium against ischemia-reperfusion injury in vivo. Methods Seventy-eight male adult SD rats weighing 270-390g were anesthetized with intraperitoneal pentobarbital sodium 50mg/kg, tracheostomized and mechanically ventilated. PaCO2 was maintained at 25-40 mm Hg. Their chests were opened and hearts exposed. I/R was produced by reversible occlusion of left anterior descending branch (LAD) of coronary artery for 30 min followed by 2h reperfusion. Seventy-eight animals were randomly divided into 13 groups (n=6): (A) sham group；Rats received no ischemic-reperfusion. (B) Simple-Ischemic group；Rats were experienced myocardium ischemia-reperfusion merely. (C) Parthenolide (PTN) group；Nuclear Factor-κB (NF-κB) inhibitor PTN (500μg/kg) was administered intraperitoneally(IP). (D) Sevoflurane-I/R group；Rats received 2.5% sevoflurane for 30 min and 15 min wash-out followed by a 30 minutes occlusion and 2h reperfusion. (E) PTN＋sevoflurane-I/R group；PTN administered IP 15 min before exposure to sevoflurane. (F) Sevoflurane-I/R＋PTN group；PTN administered IP after sevoflurane preconditioning. Myocardium sample of all groups were collected before the time of myocardial ischemia and after the time of myocardial ischemia reperfusion respectively. In addition, (G) Sevoflurane group；Rats were received 2.5% sevoflurane for 30 min and then collected myocardium sample after 165 min. NF-κB P65 was determined by Western Blot analysis. Results Myocardium sample of all groups were collected before the time of myocardial ischemia: the expression of NF-κB P65 protein was significantly up-regulated in Sevoflurane-I/R group as compared to that of the sham group. Myocardium sample of all groups were collected after myocardial ischemia reperfusion: the expression of NF-κB P65 protein was significantly up-regulated in Simple-Ischemic group than that in the sham group and the expression of NF-κB P65 protein was significantly down-regulated in Sevoflurane-I/R group, sham group, SEVO group, PTN group, SEVO-I/R＋PTN group and PTN＋SEVO-I/R group as compared to that of Simple-Ischemic group. Conclusion Sevoflurane preconditioning has protective effects on ischemia-reperfusion myocardial injury in rats. This protective effect may be involved in the activation of NF-κB P65 during sevoflurane preconditioning.