模拟微重力效应对心肌细胞一氧化氮水平的影响及其相关机制的研究

发布时间：2018-10-19 08:35

【摘要】：空间微重力导致的心肌收缩功能下降是航天医学的重要问题,其发生机制尚不清楚.采用电子自旋共振(ESR)、免疫细胞化学和核酸原位杂交等技术研究了模拟微重力效应对心肌细胞一氧化氮(NO)水平、诱导型一氧化氮合成酶(iNOS)表达的影响及其调控的信号转导途径,以探讨模拟微重力影响心肌细胞收缩功能的可能机制.结果表明,模拟微重力导致心肌细胞NO水平增高,iNOS蛋白及其mRNA表达上调;非选择性的蛋白激酶抑制剂staurosporine和选择性的蛋白激酶C(PKC)抑制剂calphostin C均可显著抑制模拟微重力下心肌细胞NO水平增高,说明模拟微重力对iNOS表达的调节至少是部分地依赖于PKC途径.结果提示,心肌细胞NO途径对模拟微重力条件敏感,该途径可能在模拟微重力影响心肌细胞收缩功能的机制中发挥重要作用.
[Abstract]:The decline of myocardial contractile function caused by microgravity is an important problem in space medicine, and its mechanism is not clear. The effects of simulated microgravity on the expression of nitric oxide (NO) and inducible nitric oxide synthase (iNOS) in cardiomyocytes were studied by electron spin resonance (ESR),) immunocytochemistry and nucleic acid in situ hybridization (ish). To explore the possible mechanism of simulated microgravity affecting the contractile function of cardiomyocytes. The results showed that simulated microgravity increased the level of NO and up-regulated the expression of iNOS protein and mRNA in cardiomyocytes. Staurosporine, a non-selective inhibitor of protein kinase, and calphostin C, a selective inhibitor of protein kinase C (PKC), could significantly inhibit the increase of NO level in cardiomyocytes under simulated microgravity, suggesting that the regulation of iNOS expression by simulated microgravity is at least partially dependent on the PKC pathway. The results suggest that the NO pathway of cardiomyocytes is sensitive to simulated microgravity conditions, and this pathway may play an important role in the mechanism of simulated microgravity affecting the contractile function of cardiomyocytes.
【作者单位】：航天医学工程研究所航天细胞与分子生物学实验室航天医学工程研究所航天细胞与分子生物学实验室航天医学工程研究所航天细胞与分子生物学实验室
【基金】：国家高技术研究发展计划(863计划)资助项目(批准号:863-2-2-2-4)
【分类号】：R852.22

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