中华麻醉学杂志
中華痳醉學雜誌
중화마취학잡지
CHINESE JOURNAL OF ANESTHESIOLOGY
2010年
8期
1009-1011
,共3页
刘少星%刘丹彦%吴会生%安民
劉少星%劉丹彥%吳會生%安民
류소성%류단언%오회생%안민
环氧化酶2抑制剂%脑%再灌注损伤
環氧化酶2抑製劑%腦%再灌註損傷
배양화매2억제제%뇌%재관주손상
Cyclooxygenase 2 inhibitors%Brain%Reperfusion injury
目的 评价帕瑞昔布钠预先给药对大鼠局灶性脑缺血再灌注损伤的影响.方法 雄性SD大鼠64只,体重250～300 g,随机分为4组(n=16):假手术组(S组)、缺血再灌注组(I/R组)、缺血再灌注+帕瑞昔布钠5 mg/kg组(P5组)和缺血再灌注+帕瑞昔布钠10 mg/kg组(P10组).I/R组、P5组和P10组采用线栓法进行脑缺血2 h.P5组和P10组在缺血前30 min时分别经颈内静脉注射帕瑞昔布钠5、10 mg/kg.再灌注24 h时进行神经功能缺陷评分,然后取脑组织,测定脑梗死体积、细胞凋亡率、Bc1-2和Bax表达,并计算Bcl-2与Bax的比值(Bcl-2/Bax).结果 与S组比较,I/R组神经功能缺陷评分、细胞凋亡率、Bcl-2及Bax表达均升高,Bcl-2/Bax降低,脑梗死体积增大(P＜0.01).与I/R组比较,P10组神经功能缺陷评分降低,P5组和P10组细胞凋亡率和Bax表达降低,脑梗死体积缩小,Bcl-2表达和Bcl-2/Bax升高(P＜0.05或0.01).与P5组比较,P10组脑梗死体积缩小,细胞凋亡率和Bax表达降低,Bcl-2表达和Bcl-2/Bax升高(P＜0.05或0.01).结论 帕瑞昔布钠预先给药可减轻大鼠局灶性脑缺血再灌注损伤,且与剂量有关,其机制与上调Bcl-2表达、下调Bax表达从而抑制细胞凋亡有关.
目的 評價帕瑞昔佈鈉預先給藥對大鼠跼竈性腦缺血再灌註損傷的影響.方法 雄性SD大鼠64隻,體重250～300 g,隨機分為4組(n=16):假手術組(S組)、缺血再灌註組(I/R組)、缺血再灌註+帕瑞昔佈鈉5 mg/kg組(P5組)和缺血再灌註+帕瑞昔佈鈉10 mg/kg組(P10組).I/R組、P5組和P10組採用線栓法進行腦缺血2 h.P5組和P10組在缺血前30 min時分彆經頸內靜脈註射帕瑞昔佈鈉5、10 mg/kg.再灌註24 h時進行神經功能缺陷評分,然後取腦組織,測定腦梗死體積、細胞凋亡率、Bc1-2和Bax錶達,併計算Bcl-2與Bax的比值(Bcl-2/Bax).結果 與S組比較,I/R組神經功能缺陷評分、細胞凋亡率、Bcl-2及Bax錶達均升高,Bcl-2/Bax降低,腦梗死體積增大(P＜0.01).與I/R組比較,P10組神經功能缺陷評分降低,P5組和P10組細胞凋亡率和Bax錶達降低,腦梗死體積縮小,Bcl-2錶達和Bcl-2/Bax升高(P＜0.05或0.01).與P5組比較,P10組腦梗死體積縮小,細胞凋亡率和Bax錶達降低,Bcl-2錶達和Bcl-2/Bax升高(P＜0.05或0.01).結論 帕瑞昔佈鈉預先給藥可減輕大鼠跼竈性腦缺血再灌註損傷,且與劑量有關,其機製與上調Bcl-2錶達、下調Bax錶達從而抑製細胞凋亡有關.
목적 평개파서석포납예선급약대대서국조성뇌결혈재관주손상적영향.방법 웅성SD대서64지,체중250～300 g,수궤분위4조(n=16):가수술조(S조)、결혈재관주조(I/R조)、결혈재관주+파서석포납5 mg/kg조(P5조)화결혈재관주+파서석포납10 mg/kg조(P10조).I/R조、P5조화P10조채용선전법진행뇌결혈2 h.P5조화P10조재결혈전30 min시분별경경내정맥주사파서석포납5、10 mg/kg.재관주24 h시진행신경공능결함평분,연후취뇌조직,측정뇌경사체적、세포조망솔、Bc1-2화Bax표체,병계산Bcl-2여Bax적비치(Bcl-2/Bax).결과 여S조비교,I/R조신경공능결함평분、세포조망솔、Bcl-2급Bax표체균승고,Bcl-2/Bax강저,뇌경사체적증대(P＜0.01).여I/R조비교,P10조신경공능결함평분강저,P5조화P10조세포조망솔화Bax표체강저,뇌경사체적축소,Bcl-2표체화Bcl-2/Bax승고(P＜0.05혹0.01).여P5조비교,P10조뇌경사체적축소,세포조망솔화Bax표체강저,Bcl-2표체화Bcl-2/Bax승고(P＜0.05혹0.01).결론 파서석포납예선급약가감경대서국조성뇌결혈재관주손상,차여제량유관,기궤제여상조Bcl-2표체、하조Bax표체종이억제세포조망유관.
Objective To investigate the effect of parecoxib pretreatment on focal cerebral ischemia-reperfusion (I/R) injury in rats. Methods Sixty-four male SD rats weighing 250-300 g were randomly divided into 4 groups ( n= 16 each): sham operation group (group S); focal cerebral I/R group; focal cerebral I/R + parecoxib 5 mg/kg group (group P5); focal cerebral I/R + parecoxib 10 mg/kg group (group P10). Focal cerebral I/R was produced by occlusion of middle cerebral artery for 2 h followed by 24 h of reperfusion. Parecoxib 5 and 10 mg/kg were injected intravenously through the internal jugular vein 30 min before ischemia in group P5 and P10 respectively. The neurologic deficit scores (NDSs) were measured at 24 h of reperfusion and then the rats were decapitated.Brains were rapidly removed for determination of the infarct volume, apoptosis rate and expression of Bcl-2 and Bax. The ratio of Bcl-2 to Bax (Bcl-2/Bax) was calculated. Results The NDSs, apoptosis rate and expression of Bcl-2 and Bax were significantly higher, Bcl-2/Bax was significantly lower, and the infarct volume was significantly larger in group I/R than in group S ( P ＜ 0.01 ). The NDSs were significantly lower in group P10, and the apoptosis rate and Bax expression were significantly lower, the infarct volume was significantly smaller, Bcl-2 expression and Bcl-2/Bax were significantly higher in group P5 and P10 than in group I/R (P ＜0.05 or 0.01). The infarct volume was significantly smaller, the apoptosis rate and Bax expression were significantly lower, and Bcl-2 expression and Bcl-2/Bax were significantly higher in group P10 than in group P5 ( P ＜ 0.05 or 0.01 ). Conclusion Pretreatment with parecoxib can attenuate focal cerebral I/R injury in a dose-dependent manner through inhibition of cell apoptosis via up-regulation of Bcl-2 expression and down-regulation of Bax expression in rats.
