CAJ | 학술논문

目的评价七氟醚后处理对大鼠心肌缺血再灌注时线粒体自噬的影响.方法清洁级健康成年雄性SD大鼠42只,体重250～ 300 g,采用随机数字表法分为3组(n=14):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(SP组).采用结扎左冠状动脉前降支30 min后恢复灌注的方法制备大鼠心肌缺血再灌注损伤模型.SP组于再灌注即刻持续吸入2.4％七氟醚15min,I/R组吸入氧浓度为33％.于再灌注2h时处死大鼠取心脏,采用1％2,3,5氯化三苯基四氮唑测定心肌梗死范围,透射电镜下观察心肌细胞超微结构,采用JC-1探针法测定线粒体膜电位,Western blot法检测LC3Ⅱ/LC3 Ⅰ、Beclin-1、p62和Parkin的表达.结果与S组比较,I/R组心肌梗死范围增加,线粒体膜电位下降,LC3Ⅱ/LC3 Ⅰ、Beclin-1和Parkin表达上调,p62表达下调(P＜0.05);与I/R组比较,SP组心肌梗死范围减少,线粒体膜电位升高,LC3Ⅱ/LC3 Ⅰ、Beclin-1、p62和Parkin表达下调(P＜0.05).结论七氟醚后处理可减轻大鼠心肌缺血再灌注损伤,其机制可能与抑制线粒体自噬的过度激活有关.
목적 평개칠불미후처리대대서심기결혈재관주시선립체자서적영향.방법 청길급건강성년웅성SD대서42지,체중250～ 300 g,채용수궤수자표법분위3조(n=14):가수술조(S조)、심기결혈재관주조(I/R조)화칠불미후처리조(SP조).채용결찰좌관상동맥전강지30 min후회복관주적방법제비대서심기결혈재관주손상모형.SP조우재관주즉각지속흡입2.4％칠불미15min,I/R조흡입양농도위33％.우재관주2h시처사대서취심장,채용1％2,3,5록화삼분기사담서측정심기경사범위,투사전경하관찰심기세포초미결구,채용JC-1탐침법측정선립체막전위,Western blot법검측LC3Ⅱ/LC3 Ⅰ、Beclin-1、p62화Parkin적표체.결과 여S조비교,I/R조심기경사범위증가,선립체막전위하강,LC3Ⅱ/LC3 Ⅰ、Beclin-1화Parkin표체상조,p62표체하조(P＜0.05);여I/R조비교,SP조심기경사범위감소,선립체막전위승고,LC3Ⅱ/LC3 Ⅰ、Beclin-1、p62화Parkin표체하조(P＜0.05).결론 칠불미후처리가감경대서심기결혈재관주손상,기궤제가능여억제선립체자서적과도격활유관.
Objective To evaluate the effects of sevoflurane postconditioning on mitophagy during myocardial ischemia-reperfusion (I/R) in rats.Methods Forty-two pathogen-free adult male SpragueDawley rats, weighing 250-300 g, were randomly divided into 3 groups (n=14 each) using a random number table: sham operation group (group S) , I/R group and sevoflurane postconditioning group (group SP).Myocardial I/R was induced by 30 min ligation of the left anterior descending branch of the coronary artery followed by 2 h of reperfusion.In group SP, 2.4％ sevoflurane was inhaled for 15 min starting from the onset of reperfusion, while 33％ oxygen was inhaled in group I/R.The rats were sacrificed at the end of reperfusion, and the hearts were removed for measurement of myocardial infarct size (by 1％ 2, 3, 5 triphenyltetrazolium chloride) , expression of LC3 Ⅱ/LC3 Ⅰ , Beclin-1, p62 and Parkin (by Western blot) ,and mitochondrial menbrane potential (by using JC-1 probe) , and for examination of the uhrastructure of cardiomyocytes (with transmission electron microscope).Results Compared with group S, the myocardial infarct size was significantly increased, mitochondrial membrane potential was decreased, the expression of LC3 Ⅱ/LC3 Ⅰ , Beclin-1 and Parkin was up-regulated, and the expression of p62 was down-regulated in group I/R.Compared with group I/R, the myocardial infarct size was significantly decreased, the mitochondrial membrane potential was increased, and the expression of LC3 Ⅱ/LC3 Ⅰ , Beclin-1, p62 and Parkin was down-regulated in group SP.Conclusion Sevoflurane postconditioning can mitigate I/R injury in rats, and inhibition of excessive activation of mitophagy may be involved in the nechanism.