中华麻醉学杂志
中華痳醉學雜誌
중화마취학잡지
CHINESE JOURNAL OF ANESTHESIOLOGY
2011年
11期
1400-1403
,共4页
武海崟%王焱林%张宗泽%饶艳%蔡孟军
武海崟%王焱林%張宗澤%饒豔%蔡孟軍
무해음%왕염림%장종택%요염%채맹군
氟比洛芬%再灌注损伤%肺%细胞凋亡
氟比洛芬%再灌註損傷%肺%細胞凋亡
불비락분%재관주손상%폐%세포조망
Flurbiprofen%Reperfusion injury%Lung%Apoptosis
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.
目的 探討氟比洛芬酯對大鼠肺缺血再灌註損傷的影響.方法 SPF級雄性健康成年SD大鼠60隻,體重250 ~ 300 g,採用隨機數字錶法,將大鼠隨機分為3組(n=20):假手術組(S組)、肺缺血再灌註組(IR組)和氟比洛芬酯組(FA組).採用阻斷左肺門60 min再灌註120 min的方法製備肺缺血再灌註模型.FA組開胸前15 min經股靜脈註射氟比洛芬酯10 mg/kg.于左肺門再灌註120 min時處死大鼠,取肺組織,計算肺濕榦重比和凋亡指數,檢測肺組織NF-κB活性、Bcl-2和Bax蛋白錶達,計算Bcl-2/Bax比,併觀察病理學結果.結果 與S組比較,IR組和FA組肺組織濕榦重比、凋亡指數和NF-κB活性增彊,Bcl-2和Bax蛋白錶達上調,IR組Bcl-2/Bax比降低,FA組Bcl-2/Bax比升高(P<0.01);與IR組比較,FA組肺組織濕榦重比、凋亡指數和NF-κB活性降低,Bax蛋白錶達下調,Bcl-2蛋白錶達上調,Bcl-2/Bax比升高(P<0.05).FA組肺組織病理學損傷較IR組減輕.結論 氟比洛芬酯可減輕大鼠肺缺血再灌註損傷,其機製與抑製NF-κB活化,改善Bcl-2和Bax平衡,從而抑製細胞凋亡有關.
목적 탐토불비락분지대대서폐결혈재관주손상적영향.방법 SPF급웅성건강성년SD대서60지,체중250 ~ 300 g,채용수궤수자표법,장대서수궤분위3조(n=20):가수술조(S조)、폐결혈재관주조(IR조)화불비락분지조(FA조).채용조단좌폐문60 min재관주120 min적방법제비폐결혈재관주모형.FA조개흉전15 min경고정맥주사불비락분지10 mg/kg.우좌폐문재관주120 min시처사대서,취폐조직,계산폐습간중비화조망지수,검측폐조직NF-κB활성、Bcl-2화Bax단백표체,계산Bcl-2/Bax비,병관찰병이학결과.결과 여S조비교,IR조화FA조폐조직습간중비、조망지수화NF-κB활성증강,Bcl-2화Bax단백표체상조,IR조Bcl-2/Bax비강저,FA조Bcl-2/Bax비승고(P<0.01);여IR조비교,FA조폐조직습간중비、조망지수화NF-κB활성강저,Bax단백표체하조,Bcl-2단백표체상조,Bcl-2/Bax비승고(P<0.05).FA조폐조직병이학손상교IR조감경.결론 불비락분지가감경대서폐결혈재관주손상,기궤제여억제NF-κB활화,개선Bcl-2화Bax평형,종이억제세포조망유관.
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.