CAJ | 학술논문

目的探讨异丙酚联合缺血预处理对大鼠肺缺血苒灌注损伤时细胞凋亡的影响.方法雄性SD大鼠50只,200～250 g,随机分为5组(n=10):假手术组(S组)、缺血再灌注组(IR组)、异丙酚组(P组)、缺血预处理组(IP组)和异丙酚+缺血预处理组(P+IP组).阻断右肺门1 h后再灌注2 h制备大鼠单肺原位热缺血再灌注模型,P组夹闭右肺门前30 min持续静脉输注异丙酚30 mg·kg-1·h-1;IP组夹闭右肺门前先进行夹闭5 min,再灌注5 min,反复3次的缺血预处理;P+IP组夹闭肺门前30 min静脉输注异丙酚30 mg·kg-1·h-1和缺血预处理.于再灌注2 h时处死大鼠,取右肺下叶肺组织,光镜下观察肺组织病理学结果 ,计算肺损伤定量评价指标(IQA);检测肺凋亡细胞,计算肺细胞凋亡指数(AI);采用免疫组化法检测Bcl-2、Bax蛋白表达;IQA、Bcl-2/Bax蛋白比值与AI作直线相关分析.结果与S组比较,IR组、P组、IP组和P+IP组再灌注后IQA、AI均明显升高,IR组Bcl-2、Bax蛋白表达上调,Bcl-2/Bax蛋白比值降低(P<0.01);与IR组比较,P组、IP组和P+IP组IQA、AI均明显降低,Bcl-2蛋白表达水平、Bcl-2/Bax蛋白比值升高,IP组、P+IP组Bax蛋白表达下调(P<0.01),P组差异无统计学意义(P>0.05);与P组和IP组比较,P+IP组IQA及AI降低,Bcl-2/Bax蛋白比值升高(P<0.05);IQA与AI呈正相关(r=0.951,P<0.01);AI与Bcl-2/Bax蛋白比值呈负相关(r=-0.851,P<0.01).结论异丙酚联合缺血预处理可通过调节Bcl-2和Bax蛋白的表达抑制细胞凋亡,减轻肺缺血再灌注损伤.
목적 탐토이병분연합결혈예처리대대서폐결혈염관주손상시세포조망적영향.방법 웅성SD대서50지,200～250 g,수궤분위5조(n=10):가수술조(S조)、결혈재관주조(IR조)、이병분조(P조)、결혈예처리조(IP조)화이병분+결혈예처리조(P+IP조).조단우폐문1 h후재관주2 h제비대서단폐원위열결혈재관주모형,P조협폐우폐문전30 min지속정맥수주이병분30 mg·kg-1·h-1;IP조협폐우폐문전선진행협폐5 min,재관주5 min,반복3차적결혈예처리;P+IP조협폐폐문전30 min정맥수주이병분30 mg·kg-1·h-1화결혈예처리.우재관주2 h시처사대서,취우폐하협폐조직,광경하관찰폐조직병이학결과 ,계산폐손상정량평개지표(IQA);검측폐조망세포,계산폐세포조망지수(AI);채용면역조화법검측Bcl-2、Bax단백표체;IQA、Bcl-2/Bax단백비치여AI작직선상관분석.결과 여S조비교,IR조、P조、IP조화P+IP조재관주후IQA、AI균명현승고,IR조Bcl-2、Bax단백표체상조,Bcl-2/Bax단백비치강저(P<0.01);여IR조비교,P조、IP조화P+IP조IQA、AI균명현강저,Bcl-2단백표체수평、Bcl-2/Bax단백비치승고,IP조、P+IP조Bax단백표체하조(P<0.01),P조차이무통계학의의(P>0.05);여P조화IP조비교,P+IP조IQA급AI강저,Bcl-2/Bax단백비치승고(P<0.05);IQA여AI정정상관(r=0.951,P<0.01);AI여Bcl-2/Bax단백비치정부상관(r=-0.851,P<0.01).결론 이병분연합결혈예처리가통과조절Bcl-2화Bax단백적표체억제세포조망,감경폐결혈재관주손상.
Objective To investigate the effects of combination of propofol and ischemic preconditioning (IP) on pneumocyte apoptosis and the mechanism involved during lung ischemia-reperfusion (IR) injury in rats.Methods Fifty male SD rats weighing 200-250 g were randomly divided into 5 groups (n = I0 each) : group Ⅰsham operation (group S); group Ⅱ IR; group Ⅲ propoful (group P); group Ⅳ IP and group Ⅴ P+ IP. The animals were anesthetized with intraperitoneul 1% pentobarbital 10 mg/kg, tracheostomized and mechanically ventilated. Lung IR was induced by occlusion of hilum of the right lung for 1 h followed by 2 h of reperfusion.performed by occlusion of hilum of the right lung for 5 min followed by 5 min of reperfusion, repeating 3 times, ischemia. The animals were killed at 2 h of reperfusion. Tissues of inferior lobe of right lung were obtained for observation of histopathulogy with light microscope and the index of quantitative assessment of histologic lung injury (IQA) was calculated. The apoptosis of pneumocytes was detected using TUNEL and apeptosis index (AI) was calculated. The expression of Bcl-2 and Bax protein in lung tissues was detected using immunohistechemical method. Correlation between IQA and AI and between Bcl-2/Bax protein ratio and AI was analyzed. Results Compared with group S, IQA and AI in the other four groups were significantly increased after reperfusion, and the expression of Bcl-2 and Bax protein was significantly increased and Bcl-2/Bax protein ratio significantly decreased in group IR (P < 0.01). Compared with group IR, 1QA and AI were significantly decreased, Bcl-2 protein expression was up-regulated and Bcl-2/Bax protein ratio was significantly increased in group P, IP and P + IP, Bax protein expression was down-regulated in group IP and P + IP (P < 0.01), but there was no significant difference in Bax protein expression between group P and IR (P > 0.05). IQA and AI were significantly lower and Bcl-2/Bax protein ratio was significantly higher in group P + IP than in group P and IP (P < 0.05). IQA was positively correlated with AI (r = 0.951, P < 0.01). AI was negatively correlated with Bcl-2/Bax protein ratio (r = -0.851, P < 0.01). Conclusion The combination of propofol and IP can inhibit pneumocyte apoptosis through regulating the expression of Bcl-2 and Bax protein and ameliorate lung IR injury.