心肌缺血-再灌注损伤与白细胞介素-1,10

Myocardial Ischemia-reperfusion Injury With Interleukin-1, 10

目的探讨白细胞介素(IL)-1,10在心肌缺血-再灌注损伤(MIRI)中的作用及作用机制。方法检索国内外相关文献资料,进行分析、整理、总结。结果 MIRI实际执行期间,是基于细胞因子(CK)的不断释放产生。对于其中的促炎因子IL-1,在期间的反应是通过介导炎症来完成,这样能实现心肌细胞凋亡以及NO合成,从而给心肌等机制带来较大损害,并加重MIRI。对于其中的抗炎因子IL-10,是基于抑制多种促炎因子、趋化因子来实现,在期间会产生下调MIRI的炎症反应,能够达到减轻MIRI的目的。结论在MIRI的过程中,IL-1心肌有致损作用,而IL-10则对心肌保护作用。

Objective To investigate the role of interleukin （IL）-I, 10 in myocardia1 ischemia-reperfusion injury （MIRI） and its mechanism. Methods The relevant literatures at home and abroad were retrieved, analyzed, so^ted and summarized. Results In the process of MIRI, accompanied oy the release of cytokines （CK）, which proinflammatory eytokines IL-1 can mediate inflammatory response, promote myocardial cell apoptosis and promote NO synthesis, direct damage to myocardium and other mechanisms to increase MIRI, and anti-inflammatory factor IL-I 0 by inhibiting a variety of proinflammatory and chemokine expression, down-regulation of MIRI inflammatory response, thereby reducing MIRI. Conclusion In the process ofMIRI, 1L-1 myoeardium has a detonation effect, while IL-10 has a protective effect on myocardium.