摘要
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-1βmRNA,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。
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.
出处
《中华急诊医学杂志》
CAS
CSCD
2005年第12期989-992,共4页
Chinese Journal of Emergency Medicine
基金
广州市科委重点攻关课题(2001-Z-130-02)
广东省医学科研基金(A2003176)
