CAJ | 학술논문

目的：探讨不同浓度的一氧化碳（CO）对缺血再灌注后心肌细胞存活率、LDH水平及活性氧（ROS）生成的影响。方法：将H9c2心肌细胞随机分为Sham组，Control组及CORM组。Control组及CORM组为缺血再灌注（氧糖剥夺3h－氧糖恢复1h）后 H9c2细胞。 CORM 组在再灌注开始时分别给予 CO 释放分子2（CORM2）20μM，40μM，60μM，80μM，100μM干预。检测各组细胞存活率、LDH水平及ROS生成。结果：CORM2浓度在20μM，40μM，60μM及80μM时，细胞ROS生成及LDH水平较Control组有明显降低，细胞存活率增加，其中以CORM240μM最为显著。当CORM2浓度为100uM，各项指标与Control组比较无统计学差异。结论：CO在有效低浓度范围内，可减少再灌注损伤心肌细胞ROS的生成，改善细胞损伤。
목적：탐토불동농도적일양화탄（CO）대결혈재관주후심기세포존활솔、LDH수평급활성양（ROS）생성적영향。방법：장H9c2심기세포수궤분위Sham조，Control조급CORM조。Control조급CORM조위결혈재관주（양당박탈3h－양당회복1h）후 H9c2세포。 CORM 조재재관주개시시분별급여 CO 석방분자2（CORM2）20μM，40μM，60μM，80μM，100μM간예。검측각조세포존활솔、LDH수평급ROS생성。결과：CORM2농도재20μM，40μM，60μM급80μM시，세포ROS생성급LDH수평교Control조유명현강저，세포존활솔증가，기중이CORM240μM최위현저。당CORM2농도위100uM，각항지표여Control조비교무통계학차이。결론：CO재유효저농도범위내，가감소재관주손상심기세포ROS적생성，개선세포손상。
Objective: To investigate the effects of different dosage carbon monoxide (CO) on myocardial cell ROS production, MTT and LDH activity after ischemia-reperfusion injury. Methods: Ischemia/reperfusion model of H9c2 (OGD3h-OGR1h) was established. H9c2 cells were randomly divided into Sham group, Control group, and different dosage CORM groups treated with CORM2 (20 μM, 40 μM, 60 μM, 80 μM, 100 μM) at the onset of reperfusion. H9c2 cell ROS production, MTT and LDH activity were detected. Results: Cell ROS production and LDH activity were significantly decreased and cell viability were evidently increased in CORM (20 μM, 40 μM, 60μM, 80 μM) groups compared with Control group. The effect of CORM40μM was relatively the most remarkable. 100μM CORM2 had no protective effect on H9c2 cells after ischemia-reperfusion. Conclusion: CO in the effective range of low concentration can provide protection to the cardiac cells subjected to ischemia/reperfusion injury by reducing cell ROS production.