白细胞介素-1β在脓毒症鼠心肌中的表达及p38MAPK的调控作用

目的探讨白细胞介素-1β（IL-1β）在脓毒症鼠心肌损伤中的作用及p38MAPK的调控机制。方法采用盲肠结扎并穿刺（CLP）来制作脓毒症模型，并在不同时相点观察大鼠血清CPK-MB、IL-1β浓度及其mRNA在心肌的表达、心肌p38MAPK的活性。结果CLP术后血清IL-1β浓度进行性升高，CPK—MB显著提高。正常心肌组织微量表达IL-1β mRNA，脓毒症时可见大量表达，且p38MAPK明显激活。血清IL-1β的水平及其mRNA在心肌中的表达与CPK-MB呈显著正相关。应用p38MAPK抑制剂SB203580后，p38MAPK激活受抑，血清IL-1β浓度显著降低，IL-1β在心肌中的表达减少，心肌损害明显减轻。结论IL-1β的大量释放及其在心肌中显著表达是脓毒症鼠心肌损伤的原因之一，而通过调控p38MAPK信号通路可对心肌起保护作用。

Expression of IL-1 beta in the septic rat's myocardial tissue and the role of p38MAPK signal pathway in septic rats

Objective To investigate the role of IL-1 beta myocardial injury and the regulatior mechanisms of p38MAPK in the septic rats. Methods Cecal ligation and puncture was adopted to build sepsis model. The level of serum CPK-MB, IL-1 beta and the expression of IL-1 betas mRNA in the myocardial cells, the activity of p38MAPK in the myocardial tissue at different time points were measured. Results The level of IL-1 beta and CK-MB increased progressively after the CLP operation. The expression of IL-1 beta was not found in normal myocardial tissue, but increased significantly in sepsis. The p38MAPK was found to be activated strongly. The level of IL-1 beta and the expression of IL- l beta RNA in the myocardial tissue showed a significant correlation with CPK-MB. After administering p38MAPK inhibitor, SB203580, the level of IL-1 beta and the expression of IL-1 beta in the myocardium were found to decrease evidently. The myocardial injury was alleviated and activation of p38 MAPK was inhibited. Conclusion Excessive release of IL-1 beta and the expression of IL-1 beta mRNA in the myocardium are the main causes of myocardial injury in septic rat. The regulation of the p38MAPK pathway may protect myocardial cells during sepsis.