CAJ | 학술논문

目的探讨细胞凋亡在体外循环(CPB)肺损伤中的作用机制.方法选取健康新西兰大白兔20只,随机分为CPB组和对照组(Sham组,单纯开胸).测定各组围CPB期左右心房中性粒细胞计数、氧合指数;取肺组织样本,电镜观察其超微结构,并动态记录肺组织含水量、细胞凋亡相关因子B淋巴细胞/白血病-2(bcl-2)、bcl-2相关X蛋白(bax)、Fas配体(FasL)的表达和bcl-2/bax及细胞凋亡指数变化.结果 CPB后,CPB组较Sham组氧合指数明显下降(P＜0.05),中性粒细胞在肺内明显聚集(P＜0.05),肺组织含水量显著增加(P＜0.05).同时,肺组织细胞凋亡指数明显升高[CPB 30 min,(51.13 ±9.87)‰比(1.27-1.03)‰,P＜0.05;CPB停止即刻,(59.64±7.74)‰比(1.30±0.82)‰,P＜0.05],肺泡上皮细胞FasL蛋白表达增加[CPB 30 min,(53.84±8.64)％比(4.25±1.41)％,P ＜0.05;CPB停止即刻,(81.88±9.67)％比(4.32±1.32)％,P＜0.05],bax蛋白表达增加[CPB 30 min,(56.78±9.12)％比(6.69±1.00)％,P＜0.05;CPB停止即刻,(77.28±8.48)％比(6.96±1.03)％,P＜0.05],bcl-2蛋白表达下降[CPB 30 min,(15.25±1.98)％比(22.87±3.15)％,P ＜0.05;CPB停止即刻,(10.35±1.67)％比(23.54±2.34)％,P＜0.05].结论体外循环可引发炎性肺损伤,并通过外源性及内源性凋亡途径诱发肺组织细胞凋亡.
목적 탐토세포조망재체외순배(CPB)폐손상중적작용궤제.방법 선취건강신서란대백토20지,수궤분위CPB조화대조조(Sham조,단순개흉).측정각조위CPB기좌우심방중성립세포계수、양합지수;취폐조직양본,전경관찰기초미결구,병동태기록폐조직함수량、세포조망상관인자B림파세포/백혈병-2(bcl-2)、bcl-2상관X단백(bax)、Fas배체(FasL)적표체화bcl-2/bax급세포조망지수변화.결과 CPB후,CPB조교Sham조양합지수명현하강(P＜0.05),중성립세포재폐내명현취집(P＜0.05),폐조직함수량현저증가(P＜0.05).동시,폐조직세포조망지수명현승고[CPB 30 min,(51.13 ±9.87)‰비(1.27-1.03)‰,P＜0.05;CPB정지즉각,(59.64±7.74)‰비(1.30±0.82)‰,P＜0.05],폐포상피세포FasL단백표체증가[CPB 30 min,(53.84±8.64)％비(4.25±1.41)％,P ＜0.05;CPB정지즉각,(81.88±9.67)％비(4.32±1.32)％,P＜0.05],bax단백표체증가[CPB 30 min,(56.78±9.12)％비(6.69±1.00)％,P＜0.05;CPB정지즉각,(77.28±8.48)％비(6.96±1.03)％,P＜0.05],bcl-2단백표체하강[CPB 30 min,(15.25±1.98)％비(22.87±3.15)％,P ＜0.05;CPB정지즉각,(10.35±1.67)％비(23.54±2.34)％,P＜0.05].결론 체외순배가인발염성폐손상,병통과외원성급내원성조망도경유발폐조직세포조망.
Objective To study the effect of apoptosis on lung injury after cardiopulmonary bypass (CPB).Methods Twenty New Zealand rabbits were selected and randomly divided into two groups:CPB group undergoing CPB; Sham group only receiving open chest operation.Blood neutrophils count from right and left atrium and oxygenation index in the two groups were determined perioperatively.Lung water content,bcl-2 protein,bax protein,Fas ligand (FasL) protein,bcl-2/bax,apoptosis index and pathomorphological changes were measured in the lung tissues.Results After CPB,as compared with Sham group,the lung water content (P ＜ 0.05),neutrophils count (P ＜ 0.05) and oxygenation index (P ＜ 0.05) were significantly elevated in CPB group.Moreover,CPB could increase the expression of FasL (CPB 30 min,53.84±8.64 vs.4.25 ± 1.41,P＜0.05; CPB termination,81.88 ±9.67 vs.4.32 ± 1.32,P＜0.05) and bax (CPB 30 min,56.78 ±9.12 vs.6.69 ± 1.00,P＜0.05; CPB termination,77.28 ±8.48 vs.6.96 ± 1.03,P ＜ 0.05) on alveolar epithelial cells and decrease the expression of bcl-2 (CPB 30 min,15.25 ± 1.98 vs.22.87 ± 3.15,P ＜ 0.05 ; CPB termination,10.35 ± 1.67 vs.23.54 ± 2.34,P ＜ 0.05) and could also promote pathomorphological changes in the lung tissue.Conclusion CPB can induce inflammation of lung tissue and apoptosis through the endogenous and exogeneous apoptosis pathways.