氟比洛芬酯对大鼠肺缺血再灌注损伤的影响

目的 探讨氟比洛芬酯对大鼠肺缺血再灌注损伤的影响.方法 SPF级雄性健康成年SD大鼠60只,体重250 ～ 300 g,采用随机数字表法,将大鼠随机分为3组(n=20):假手术组(S组)、肺缺血再灌注组(IR组)和氟比洛芬酯组(FA组).采用阻断左肺门60 min再灌注120 min的方法制备肺缺血再灌注模型.FA组开胸前15 min经股静脉注射氟比洛芬酯10 mg/kg.于左肺门再灌注120 min时处死大鼠,取肺组织,计算肺湿干重比和凋亡指数,检测肺组织NF-κB活性、Bcl-2和Bax蛋白表达,计算Bcl-2/Bax比,并观察病理学结果.结果 与S组比较,IR组和FA组肺组织湿干重比、凋亡指数和NF-κB活性增强,Bcl-2和Bax蛋白表达上调,IR组Bcl-2/Bax比降低,FA组Bcl-2/Bax比升高(P＜0.01)；与IR组比较,FA组肺组织湿干重比、凋亡指数和NF-κB活性降低,Bax蛋白表达下调,Bcl-2蛋白表达上调,Bcl-2/Bax比升高(P＜0.05).FA组肺组织病理学损伤较IR组减轻.结论 氟比洛芬酯可减轻大鼠肺缺血再灌注损伤,其机制与抑制NF-κB活化,改善Bcl-2和Bax平衡,从而抑制细胞凋亡有关.

Effect of flurbiprofen axetil on lung ischemia-reperfusion injury in rats

Objective To investigate the effect of flurbiprofen axetil on lung ischemia-reperfusion(I/R) injury in rats.Methods Sixty healthy male SD rats weighing 250-300 g were randomly divided into 3 groups( n =20 each): group sham operation(group S) ;group I/R and group flurbiprofen axetil (group FA).The animals were anesthetized with intraperitoneal 2％ pentobarbital 50 mg/kg and tracheostomized and mechanically ventilated.Lung I/R was induced by 60 min occlusion of left hilus pulmonis followed by 120 min reperfusion.In FA group flurbiprofen axetil 10 mg/kg was injected iv at 15 min before occlusion of left hilus pulmonis.The rats were sacrificed at 120 min of reperfusion and then the lungs were removed for measurement of lung wet/dry weight ratio,apoptosis index,NF-κB activity,Bcl-2 and Bax protien expression,and microscopic examination.Bcl-2/Bax ratio was caculated.Results I/R significantly increased lung wet/dry weight ratio,apoptosis index,NF-κB activity,Bcl-2 and Bax protien expression,and decreased Bcl-2/Bax ratio.Flurbiprofen axetil preconditioning significantly attenuated the I/R-induced changes in lung wet/dry weight ratio,apoptosis index,NF-κB activity,Bcl-2 and Bax protien expression,and Bcl-2/Bax ratio in group FA as compared with group I/R.Flurbiprofen axetil preconditioning also ameliorated I/R-induced lung damage.Conclusion Flurbiprofen axetil can attenuate lung I/R injury in rats by inhibiting NF-κB activity,up-regulating Bcl-2 expression and down-regulating Bax expression and inhibiting apoptosis.