CAJ | 학술논문

目的分析大鼠乳鼠心肌细胞经历缺氧预处理后miRNA的表达谱变化，探索其缺氧预处理机制和治疗靶点。方法大鼠乳鼠心肌细胞原代培养，经过缺氧预处理和缺氧复氧损伤后检验心肌细胞存活率和乳酸脱氢酶浓度，miRNA芯片技术检测正常心肌和缺氧预处理心肌细胞miRNA表达谱差异，实时定量PCR验证结果的可信性，分析明显差异表达的miRNA的生物学功能。结果心肌细胞存活率和乳酸脱氢酶浓度结果证实缺氧预处理模型制备成功。miRNA芯片技术结果表明，与正常对照组心肌细胞相比，缺氧预处理心肌细胞中有6个miRNA表达上调，有5个表达下调，其中一部分miRNA的生物学功能与心血管功能相关。结论缺氧预处理可导致大鼠乳鼠心肌细胞microRNA表达谱发生变化，其可能是缺氧复氧损伤潜在的治疗靶点。
목적 분석대서유서심기세포경력결양예처리후miRNA적표체보변화，탐색기결양예처리궤제화치료파점。방법 대서유서심기세포원대배양，경과결양예처리화결양복양손상후검험심기세포존활솔화유산탈경매농도，miRNA심편기술검측정상심기화결양예처리심기세포miRNA표체보차이，실시정량PCR험증결과적가신성，분석명현차이표체적miRNA적생물학공능。결과 심기세포존활솔화유산탈경매농도결과증실결양예처리모형제비성공。miRNA심편기술결과표명，여정상대조조심기세포상비，결양예처리심기세포중유6개miRNA표체상조，유5개표체하조，기중일부분miRNA적생물학공능여심혈관공능상관。결론 결양예처리가도치대서유서심기세포microRNA표체보발생변화，기가능시결양복양손상잠재적치료파점。
Objective]To analyze the changes of miRNA expression profile in cardiomyocytes of neonate rats after hypoxia preconditioning ,and to explore the mechanism of hypoxia preconditioning and therapeutic target .[Methods]Pri‐mary cardiomyocytes of neonate rats were cultured .Survival rate of rat cardiomyocytes and lactate dehydrogenase(LDH) level were detected after hypoxia preconditioning and hypoxia reoxygenation .The expression profiles of miRNA in normal and hypoxia preconditioned cardiomyocytes were detected by miRNA genetic chip .The results were verified by real‐time quantitative polymerase chain reaction(PCR) ,and the biological function of miRNA significantly differentially expressed were analyzed .[Results]The successful establishment of hypoxia preconditioning models was verified by the results of sur‐vival rate of rat cardiomyocytes and LDH levels .The miRNA chip detection results showed that 6 miRNAs in hypoxia preconditioned cardiomyocytes were up‐regulated and 5 miRNAs were down‐regulated in comparison with normal cardio‐myocytes .The biological function of some miRNAs was related to cardiovascular function .[Conclusion]Hypoxia precon‐ditioning leads to the changes of miRNA expression profile which may serve as potential targets for the treatment of hy‐poxia reoxygenation injury .