CAJ | 학술논문

目的评价卡托普利和异氟醚联合预处理对兔心肌缺血再灌注时细胞凋亡的影响.方法新西兰大白兔40只,雌雄不拘,体重1.8 ～ 2.5 kg,采用随机数字表法,将其分为5组(n=8):假手术组(S组)、缺血再灌注组(I/R组)、异氟醚预处理组(I组)、卡托普利预处理组(C组)、卡托普利和异氟醚联合预处理组(C+I组).I/R组、I组、C组和C+I组采用结扎冠状动脉左前降支法制备心肌缺血再灌注损伤模型.I组吸入1.1％异氟醚30 min,洗脱15 min,然后进行心肌缺血.C组给予卡托普利25 mg/kg灌胃,24h后进行心肌缺血.C+I组给予卡托普利25 mg/kg灌胃,24h后吸入1.1％异氟醚30 min,洗脱15 min,然后进行心肌缺血.再灌注结束时处死兔,取心肌组织,光镜下观察病理学结果,电镜下观察超微结构,采用流式细胞术检测心肌细胞凋亡率,采用Western blot法测定Bcl-2和Bax的蛋白表达水平,计算Bcl-2与Bax的比值(Bcl-2/Bax).结果与S组比较,I/R组、I组、C组和C+I组细胞凋亡率升高,Bcl-2和Bax的蛋白表达上调,Bcl-2/Bax降低(P＜0.05).与I/R组、I组和C组比较,C+I组细胞凋亡率降低,Bcl-2蛋白表达上调,Bax蛋白表达下调,Bcl-2/Bax升高(P＜0.05),病理学损伤减轻.结论异氟醚和卡托普利联合预处理减轻兔心肌缺血再灌注损伤的机制可能与其调节Bcl-2/Bax平衡,抑制心肌细胞凋亡有关.
목적 평개잡탁보리화이불미연합예처리대토심기결혈재관주시세포조망적영향.방법 신서란대백토40지,자웅불구,체중1.8 ～ 2.5 kg,채용수궤수자표법,장기분위5조(n=8):가수술조(S조)、결혈재관주조(I/R조)、이불미예처리조(I조)、잡탁보리예처리조(C조)、잡탁보리화이불미연합예처리조(C+I조).I/R조、I조、C조화C+I조채용결찰관상동맥좌전강지법제비심기결혈재관주손상모형.I조흡입1.1％이불미30 min,세탈15 min,연후진행심기결혈.C조급여잡탁보리25 mg/kg관위,24h후진행심기결혈.C+I조급여잡탁보리25 mg/kg관위,24h후흡입1.1％이불미30 min,세탈15 min,연후진행심기결혈.재관주결속시처사토,취심기조직,광경하관찰병이학결과,전경하관찰초미결구,채용류식세포술검측심기세포조망솔,채용Western blot법측정Bcl-2화Bax적단백표체수평,계산Bcl-2여Bax적비치(Bcl-2/Bax).결과 여S조비교,I/R조、I조、C조화C+I조세포조망솔승고,Bcl-2화Bax적단백표체상조,Bcl-2/Bax강저(P＜0.05).여I/R조、I조화C조비교,C+I조세포조망솔강저,Bcl-2단백표체상조,Bax단백표체하조,Bcl-2/Bax승고(P＜0.05),병이학손상감경.결론 이불미화잡탁보리연합예처리감경토심기결혈재관주손상적궤제가능여기조절Bcl-2/Bax평형,억제심기세포조망유관.
Objective To evaluate the effect of captopril and isoflurane preconditioning on cell apoptosis during myocardial ischemia/reperfusion (I/R) in rabbits.Methods Forty New Zealand white rabbits of both sexes,weighing 1.8-2.5 kg,were randomly divided into 5 groups (n =8 each) using a random number table:sham operation group (group S),group I/R,isoflurane preconditioning group (group I),captopril preconditioning group (group C) and captopril and isoflurane preconditioning group (group C + I).The animals were anesthetized with 3％ pentobarbital sodium 30 mg/kg.Myocardial ischemia was induced by occlusion of the left anterior descending branch of coronary artery for 30 min followed by 120 min of reperfusion.1.1％ isoflurane was inhaled for 30 min followed by 15 min washout before myocardial ischemia in group I.Captopril 25 mg/kg was given through a gastric tube into the stomach at 24 h before myocardial ischemia in group C.Captopril 25 mg/kg was given through a gastric tube into the stomach,24 h later 1.1％ isoflurane was inhaled for 30 min followed by 15 min washout,and then myocardial ischemia was performed in group C + I.The rabbits were sacrificed at the end of reperfusion and myocardial specimens were removed for microscopic examination and observation of ultrastructure,and for determination of the expression of Bcl-2 and Bax proteins (by Western blot).The apoptosis rate was detected by flow cytometry.Bcl-2/Bax ratio was calculated.Results Compared with group S,the apoptosis rate was significantly increased,the expression of Bcl-2 and Bax proteins was up-regulated,and Bel-2/Bax ratio was decreased in I/R,I,C and C + I groups (P ＜ 0.05).Compared with I/R,I and C groups,the apoptosis rate was significantly decreased,Bcl-2 protein expression was up-regulated,Bax protein expression was down-regulated,and Bcl-2/Bax ratio was increased (P ＜ 0.05),and the pathological changes were significantly attenuated in group C + I.Conclusion Regulation of Bcl-2/Bax ratio and inhibition of apoptosis in myocardial cells are involved in the mechanism by which isoflurane and captopril preconditioning reduces I/R injury in rabbits.