CAJ | 학술논문

目的评价七氟醚后处理对大鼠心肌缺血再灌注时心肌细胞凋亡的影响.方法健康雄性Wistar大鼠45只,体重250～ 280 g,采用随机数字表法,将大鼠随机分为3组(n=15):假手术组(S组)、心肌缺血再灌注组(I/R组)和七氟醚后处理组(Spo组).I/R组和Spo组采用结扎左冠状动脉前降支30 min时进行再灌注120 min的方法制备心肌缺血再灌注损伤模型,S组仅在左冠状动脉前降支下穿线.Spo组进行七氟醚后处理,于再灌注前1 min时吸八七氟醚,呼气末浓度2.5％,持续5min.于再灌注120 min时取左室心肌组织,测定缺血危险区和梗死区体积,计算缺血危险区和梗死区体积百分比.取左室缺血危险区心肌组织,测定心肌细胞凋亡指数,测定凋亡相关蛋白Bcl-2和Bax的蛋白及其mRNA的表达,计算Bcl-2/Bax比值.结果与S组比较,I/R组心肌梗死区体积百分比和心肌细胞凋亡指数升高,Bcl-2、Bax蛋白及mRNA表达上调,Bcl-2/Bax比值降低(P＜0.05)；与I/R组比较,Spo组心肌梗死区体积百分比和心肌细胞凋亡指数降低,Bax蛋白及mRNA表达下调,Bcl-2蛋白及mRNA表达上调,Bcl-2/Bax比值升高(P＜0.05).结论七氟醚后处理通过上调Bcl-2表达,下调BBax表达,改善Bcl-2/Bax平衡,抑制心肌细胞凋亡,从而减轻大鼠心肌缺血再灌注损伤.
목적 평개칠불미후처리대대서심기결혈재관주시심기세포조망적영향.방법 건강웅성Wistar대서45지,체중250～ 280 g,채용수궤수자표법,장대서수궤분위3조(n=15):가수술조(S조)、심기결혈재관주조(I/R조)화칠불미후처리조(Spo조).I/R조화Spo조채용결찰좌관상동맥전강지30 min시진행재관주120 min적방법제비심기결혈재관주손상모형,S조부재좌관상동맥전강지하천선.Spo조진행칠불미후처리,우재관주전1 min시흡팔칠불미,호기말농도2.5％,지속5min.우재관주120 min시취좌실심기조직,측정결혈위험구화경사구체적,계산결혈위험구화경사구체적백분비.취좌실결혈위험구심기조직,측정심기세포조망지수,측정조망상관단백Bcl-2화Bax적단백급기mRNA적표체,계산Bcl-2/Bax비치.결과 여S조비교,I/R조심기경사구체적백분비화심기세포조망지수승고,Bcl-2、Bax단백급mRNA표체상조,Bcl-2/Bax비치강저(P＜0.05)；여I/R조비교,Spo조심기경사구체적백분비화심기세포조망지수강저,Bax단백급mRNA표체하조,Bcl-2단백급mRNA표체상조,Bcl-2/Bax비치승고(P＜0.05).결론 칠불미후처리통과상조Bcl-2표체,하조BBax표체,개선Bcl-2/Bax평형,억제심기세포조망,종이감경대서심기결혈재관주손상.
Objective To investigate the effects of sevoflurane postconditioning on cardiomyocyte apoptosis during myocardial ischemia-repeffusion (I/R) in rats.Methods Forty-five healthy male Wistar rats weighing 250-280 g were randomly divided into 3 groups ( n =15 each):group sham operation ( group S) ; group I/R and group sevoflurane postconditioning (group Spo).The animals were anesthetized with intraperitoneal 3％ pentobarbital 45 mg/kg,tracheally intubated and mechanically ventilated.Myocardial I/R was produced by occlusion of anterior descending branch of left coronary artery for 30 min followed by 120 min reperfusion in groups I/R and Spo.In group Spo the animals inhaled 2.5％ sevoflurane for 5 min starting from 1 min before reperfusion was started.The animals were sacrificed at the end of 120 min reperfusion.Their hearts were removed for measurement of infarct size and the area at risk and determination of apoptotic index (the number of apoptotic cells/the total number of cells) and Bcl-2 and Bax protein and mRNA expression.Results Sevoflurane postconditioning significantly reduced infarct size in group Spo as compared with group I/R.There was no significant difference in area at risk between groups I/R and Spo.Myocardial I/R significantly increased the apoptotic index,Bcl-2 and Bax protein and mRNA expression in group I/R as compared with group S.Sevoflurane postconditioning significantly decreased apoptotic index and Bax protein and mRNA expression but increased Bcl-2 protein and mRNA expression in group Spo as compared with group I/R.Conclusion Sevoflurane postconditioning attenuates myocardial I/R injury by redncing myocardial apoptosis,up-regulating Bcl-2 expression and down-regulating Bax expression.