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目的:探讨一氧化碳释放分子(CORM-2)对心肌细胞缺氧的保护作用及其机制。方法:将大鼠心肌细胞H9C2分为4组:正常组(H9C2)、缺氧组(Hypoxia+H9C2)、CORM-2组(CORM-2+Hypoxia+H9C2)和iCORM-2组(iCORM-2+Hypoxia+H9C2)。CCK-8和流式细胞术分别检测心肌细胞活性和凋亡情况;免疫荧光检测HMGB1核浆分布情况;Western Blot检测心肌细胞胞浆内HMGB1表达和总HMGB1的表达情况,以及相关凋亡蛋白表达。结果:缺氧组与正常组比较,细胞活性下降,凋亡率增高(9.5%vs 27.4%,P<0.05),胞浆HMGB1迁移增加,细胞总HMGB1及凋亡相关蛋白表达增加(P<0.05)。CORM-2组与缺氧组相比,细胞的活性升高(P<0.05),凋亡率降低至14.1%,胞浆HMGB1释放量及总表达量减少,Cleaved Caspase-3表达降低,ICORM-2组与缺氧组无明显变化。结论:CORM-2通过影响HMGB1分布及表达减轻心肌细胞缺氧损伤。
Objective: To investigate the protective effect of carbon monoxide releasing molecule (CORM-2) on cardiomyocytes hypoxia and its mechanism. Methods: H9C2 was divided into 4 groups: H9C2, Hypoxia + H9C2, CORM-2 + Hypoxia + H9C2 and iCORM-2 + Hypoxia + H9C2). The activity and apoptosis of cardiomyocytes were detected by CCK-8 and flow cytometry. The distribution of HMGB1 nuclear plasmids was detected by immunofluorescence. The expression of HMGB1 and HMGB1 in the cytoplasm of cardiomyocytes were detected by Western Blot and the expression of related apoptosis proteins . Results: Compared with the normal group, the cell viability decreased and the apoptosis rate increased (9.5% vs 27.4%, P <0.05). The migration of HMGB1 in cytoplasm increased and the expression of HMGB1 and apoptosis related proteins increased ). Compared with hypoxic group, CORM-2 group had higher cell viability (P <0.05), apoptosis rate decreased to 14.1%, cytoplasmic HMGB1 release and total expression decreased, Cleaved Caspase-3 expression decreased, ICORM- There was no significant change between the two groups and the hypoxia group. Conclusion: CORM-2 attenuates cardiomyocyte hypoxia injury by affecting the distribution and expression of HMGB1.