中国组织工程研究

中国组织工程研究 ›› 2011, Vol. 15 ›› Issue (28): 5277-5280.doi: 10.3969/j.issn.1673-8225.2011.28.037

• 肌肉肌腱韧带组织构建 tissue construction of the muscle, tendon and ligament • 上一篇    下一篇

环磷酸腺苷和一氧化氮在后适应保护缺氧/复氧损伤心肌细胞中的作用

王  茜1，刘革修2，宾  娟1，徐江平1   

  1. 1南方医科大学药学院神经药理课题组，广东省广州市  510515
    2 暨南大学医学院血液病研究所，广东省广州市  510632
  • 收稿日期:2011-04-01 修回日期:2011-05-02 出版日期:2011-07-09 发布日期:2011-07-09
  • 通讯作者: 徐江平，教授，博士生导师，南方医科大学药学院神经药理课题组，广东省广州市 510515 jpx@fimmu.com
  • 作者简介:王茜☆，女，1974年生，湖南省益阳市人，汉族，南方医科大学在读博士，主要从事心血管药理学研究。 wangqian86@ hotmail.com

Cyclic adenosine monophosphate and nitric oxide in protection of postconditioning from hypoxia/reoxygenation injury in cultured cardiomyocytes

Wang Qian1, Liu Ge-Xiu2, Bin Juan1, Xu Jiang-Ping1   

  1. 1Department of Pharmacology, School of Pharmaceutical Sciences, Southern Medical University, Guangzhou 510515, Guangdong Province, China
    2Institute of Hematology, School of Medicine, Jinan University, Guangzhou 510632, Guangdong Province, China
  • Received:2011-04-01 Revised:2011-05-02 Online:2011-07-09 Published:2011-07-09
  • Contact: Xu Jiang-ping, Professor, Doctoral supervisor, Department of Pharmacology, School of Pharmaceutical Sciences, Southern Medical University, Guangzhou 510515, Guangdong Province, China jpx@fimmu.com
  • About author:Wang Qian☆, Studying for doctorate, Department of Pharmacology, School of Pharmaceutical Sciences, Southern Medical University, Guangzhou 510515, Guangdong Province, China wangqian86@ hotmail.com

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被引次数

3

摘要：

背景：周期性的环磷酸腺苷浓度改变参与了预适应对缺血心脏的保护作用。
目的：观察环磷酸腺苷和一氧化氮在缺氧/复氧心肌细胞后适应保护机制中的可能作用。
方法：原代培养SD乳鼠心肌细胞，随机分为11组分别处理：正常对照组、缺氧/复氧组、心肌缺血后适应组、心肌缺血后适应+咯利普兰组、心肌缺血后适应+SQ22536或左旋精氨酸+心肌缺血后适应组，咯利普兰、SQ22536或各浓度Nω-硝基精氨酸+缺氧/复氧组。
结果与结论：心肌缺血后适应能显著改善缺氧/复氧损伤造成的心肌细胞活力下降，减少乳酸脱氢酶、肌酸激酶的释放，降低一氧化氮、肿瘤坏死因子α和白细胞介素β的mRNA表达；咯利普兰能进一步增强后适应对心肌细胞的保护作用，而腺苷酸环化酶抑制剂SQ22536可显著减弱该作用；20，100 μmol/L 非选择性一氧化氮合酶抑制剂Nω-硝基-左旋精氨酸能发挥类似于后适应的保护作用，而在1 000 μmol/L时则损伤心肌细胞(P < 0.05)。证实心肌缺血后适应对缺氧/复氧损伤心肌细胞的保护，可能是通过增强环磷酸腺苷信号抑制炎症过程实现的。

关键词: 缺血再灌注, 缺血后适应, 环磷酸腺苷, 一氧化氮, 炎症 

Abstract:

BACKGROUND: Previous studies have shown cyclic increases in tissue cyclic adenosine monophosphate (cAMP) during a multiple-cycle preconditioning protocol and the possibility that cAMP acts as a messenger or signal to elicit protection to subsequent ischemic damage.
OBJECTIVE: To investigate the possible effects of cAMP and nitric oxide (NO) in the postconditioning protection of the cardiomyocytes from hypoxia/reoxygenation (H/R) injury.
METHODS: Primary cultured Sprague-Dawley neonatal rat cardiomyocytes were randomly divided into 11 groups: normal control, H/R, postconditioning, postconditioning+rolipram, postconditioning+SQ22536 or L-arginine+ postconditioning, rolipram, SQ22536 or Nω-nitro-L-arginine (L-NAME)+H/R.
RESULTS AND CONCLUSION: Ischemic postconditioning significantly improved cell viability, reduced lactate dehydrogenase and creatine kinase release, decreased expression of nitric oxide, tumor necrosis factor-α, and interleukin-β. The specific PDE4 inhibitor rolipram could further strength the protective effect of ischemic postconditioning on cardiomyocytes, while the specific adenylyl cyclase inhibitor SQ22536 could significantly attenuate this effect (P < 0.05). A non-selective nitric oxide synthase inhibitor L-NAME showed the deleterious effect at 1000 μmol/L, while it produced similar effect to ischemic postconditioning at 20 or 100 μmol/L. These findings suggest that the cAMP and NO signaling molecules participate in the protection of postconditioning to cardiomyocytes from H/R injury, and the effect may be associated with regulation of inflammatory process.

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