白细胞介素-1,8,10与心肌缺血-再灌注损伤

Interleukin-1,8,10 and Myocardial Ischemia-Reperfusion Injury

目的探究白细胞介素(IL)-1,8,10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。结果在MIRI的过程中,伴随着细胞因子(CK)的大量释放,其中促炎因子IL-1和IL-8可通过介导炎症反应,促进心肌细胞凋亡以及促进NO合成,直接损害心肌等机制加重MIRI。而抗炎因子IL-10则通过抑制多种促炎因子和趋化因子的表达,下调MIRI的炎症反应,从而减轻MIRI。结论在MIRI的过程中,IL-1和IL-8对心肌有致损作用,而IL-10则具心肌保护作用。

Objective To explore the effect and possible mechanism of interleukin（IL）-1,8 and 10 in myocardial ischemia-reperfusion injury（MIRI）. Methods To analyze,tidy up and summarize the datum by searching for internal and external pertinent materials. Results During MIRI,lots of cytokine（CK） are highly released, and inflammatory,such as, CK IL-1 and IL-8 may injure myocardium and produce of NO by promoting inflammatory response and cardiomyocytes apoptosis. On the contrary, antiinflammatory CK IL-10 may reduce MIRI by inhibiting the production of many kinds of inflammatory CK. Conclusion In the process of MIRI, IL-1 and IL-8 may cause myocardial injury, but IL-10 has myocardial protective effect.