CAJ | 학술논문

目的：探讨硫化氢( H2 S)能否抑制离体灌流大鼠急性心肌缺血所致细胞凋亡。方法应用Langendorff 离体灌流大鼠心脏复制急性心肌缺血损伤模型,结扎冠状动脉,心肌缺血4 h。40只♂SD大鼠随机分为5组( n=8)：假手术组( Sham),缺血组( Ischemia )和硫氢化钠( NaHS )5、10、20μmol·L-1组。 HE染色分析左心室心肌细胞组织形态学变化,TUNEL 方法检测细胞凋亡, Western blot 检测各组caspase-3和Cyt-C 的蛋白表达。结果离体心肌缺血4 h后,光镜下可见心肌较大范围局灶性病变,细胞呈凝固性或带状坏死；心肌细胞凋亡率及心肌组织中caspase-3和Cyt-C蛋白表达明显升高。经NaHS 2 h处理,NaHS组光镜下心肌细胞结构清晰,心肌病变的程度明显减轻,大鼠心肌组织Cyt-C蛋白表达明显低于 Ischemia 组；NaHS 10、20μmol · L-1组心肌细胞凋亡率及心肌组织caspase-3蛋白表达明显低于Ischemia组。结论 H2 S可通过抑制细胞凋亡对离体灌流大鼠急性心肌缺血发挥一定保护作用。
목적：탐토류화경( H2 S)능부억제리체관류대서급성심기결혈소치세포조망。방법응용Langendorff 리체관류대서심장복제급성심기결혈손상모형,결찰관상동맥,심기결혈4 h。40지♂SD대서수궤분위5조( n=8)：가수술조( Sham),결혈조( Ischemia )화류경화납( NaHS )5、10、20μmol·L-1조。 HE염색분석좌심실심기세포조직형태학변화,TUNEL 방법검측세포조망, Western blot 검측각조caspase-3화Cyt-C 적단백표체。결과리체심기결혈4 h후,광경하가견심기교대범위국조성병변,세포정응고성혹대상배사；심기세포조망솔급심기조직중caspase-3화Cyt-C단백표체명현승고。경NaHS 2 h처리,NaHS조광경하심기세포결구청석,심기병변적정도명현감경,대서심기조직Cyt-C단백표체명현저우 Ischemia 조；NaHS 10、20μmol · L-1조심기세포조망솔급심기조직caspase-3단백표체명현저우Ischemia조。결론 H2 S가통과억제세포조망대리체관류대서급성심기결혈발휘일정보호작용。
Aim To investigate whether hydrogen sul-fide ( H2 S ) inhibits cardiomyocyte apoptosis induced by acute myocardial ischemia in isolated perfused rat heart. Methods The myocardial ischemia injury model was replicated with Langendorff isolated perfused rat heart, and the left anterior descending coronary ar-tery was ligated for 4 h. 40 male SD rats were divided into five groups randomly: sham group, ischemia group, and NaHS groups (5,10,20μmol·L-1). The segmental heart samples were used for HE staining. Cardiomyocyte apoptosis was detected with TUNEL as-say. The expressions of caspase-3 and Cyt-C in hearts were determined with Western blot analysis. Results Myocardial cells were found to show serious disorder and coagulated zonal necrosis under light microscope, the apoptotic rate of cardiomyocytes and the expression of caspase-3 and Cyt-C were significantly increased af-ter ischemia for 4h. Perfusion of NaHS resulted in more clear cell morphology and milder pathologic chan-ges of myocardiocytes according to the HE staining a-nalysis, and the significant decrease of expression of Cyt-C. After perfusion of 10,20 μmol·L-1 NaHS,the apoptotic rate of cardiomyocytes and the expression of caspase-3 were significantly decreased. Conclusion H2 S has certain protective effects on acute myocardial ischemic injury in isolated perfused rat heart via inhibi-ting cardiomyocyte apoptosis.