摘要目的 观察七氟烷预处理对缺血/再灌(ischemia/reperfusion,I/R)损伤大鼠心肌磷酸化抑制蛋白(phosphorylation inhebitory kappaB,p-IκBα)的影响,从另一角度进一步探讨NF-κB在七氟烷预处理中的保护机制.方法 SD雄性大鼠56只,建立大鼠心肌I,R损伤在体模型,随机分为7组:假手术组(CON组);单纯缺血组(I/R组)进行30 min心肌缺血后再灌注120min;七氟烷组(SEVO组)于吸入1.0 MAC七氟烷30 min,继之15 min药物排出后进行心肌I/R;SEVO 165'组吸人七氟烷30min后停止吸人165 min;小白菊内酯(parthenolide,PTN)组于缺血前60 min腹腔内注射NF-κβ特异性抑制剂PTN 500 μg/kg;PTN+SEVO组、SEVO+PTN组分别于七氟烷预处理前15 min、预处理后即刻腹腔内注射PTN 500 μg/kg.分别于大鼠心肌I/R前、后或相应时间点取心肌标本,采用Western blotting法测定p-IκBa的蛋白表达.结果 缺血前即刻:SEVO组(22±3)和SEVO 165'组(20±4)较CON组(15±3)p-IκBα蛋白表达上调(P<0.05);再灌注2 h后即刻:I/R组(44±6)和SEVO组(30±3)较CON组(15±4)p-IκBα蛋白表达均上调(P<0.05),而与I/R组相比,SEVO组p-IκBα蛋白上调幅度减小(P<0.05).结论 七氟烷预处理早期p-IκBα蛋白的表达上调,反馈性抑制了I/R后p-IκBα蛋白的表达,该作用可被PTN所阻断.从另一角度进一步论证了NF-κB参与七氟烷预处理的心肌保护机制.

abstractsObjective To observe the effect of sevoflurane preconditioning on the expression of p-IκBα in a rat model of myocardial ischemia-reperfusion (I/R). Methods Eighty -four male SD rats after setting up the model of I/R, randomly were divided into seven groups: ①Control group; ② Simple-Ischemic group received 30 min I/R merely; ③ SEVO group inhaled 1.0 MAC sevoflurane for 30 min and 15 min wash-out followed by a 30 min I/R; ④ SEVO 165' group inhaled 1.0 MAC sevoflurane for 30 min and then stoped for 165 min; ⑤ PTN group received PTN 500 μg/kg(NF-κB inhibitor) intraperitoneally 60 min before I/R; ⑥ PTN±SEVO group and⑦SEVO+PTN group received PTN 500 μg/kg 15 min before and after sevoflurane preconditioning. Myocardium sample of all groups were collected before and after the time of I/R or the corresponding point in time. p- IκBα was determined by Western Blotting. Results The expression of p- IκBαwas significantly up-regulated in SEVO group(22±3)and SEVO 165'group(20±4) than that in Control group (15±3) before I/R(P<0.05); After perfusion the expression of p- IκBαin Simple-Ischemic group(44±6)and SEVO group (30±3) was significantly up-regulated than that in Control group( 15±4,P<0.05);but the up-regulated adjustment of SEVO group was smaller than that in Simple-Ischemic group (P<0.05). Conclusion This study further confirmed NF-κB participates in the I/R injury and it may play an important role in the mechanism of sevoflurane-induced cardioprotection.