实验性脑出血后ICAM-1和IL-1β的表达与p38MAPK通路关系研究

Expression of ICAM-1 and IL-1β is attenuated by blocking p38MAPK after ICH in Rats

目的探讨脑出血后血肿周围组织p38丝裂原活化蛋白激酶(p38MAPK)在脑出血血肿周围组织炎性因子表达的关系。方法健康雄性Wistar大鼠30只,将动物随机分成脑出血加SB203580组和脑出血组,采用免疫组织化学方法观察干预前后不同时间点细胞间黏附分子-1(ICAM-1)和白介素-1β(IL-1β)的变化。结果免疫组化染色显示SB203580干预组ICAM-1、IL-1β在大鼠脑出血血肿周围组织中的表达均较对照组明显降低,差异有显著意义。结论 SB203580抑制IL-1β和ICAM-1的表达,p38MAPK信号通路在脑出血后血肿周围组织损伤中发挥重要的作用。

Objective ITo investigate the role of p38MAPK signal transduction pathway in the production of the proinflammatory factors such as ICAM-1 and IL-1β after intracerebral hemorrhage （ICH）. Methods 30 healthy male Wistar rats were divided into SB203580-treated group and ICH group of different time. The expression of ICAM-1 and IL-1β af- ter ICH was detected by immunohistochemical method. Results The expressions of IL-1β and ICAM-1 were significantly decreased in SB203580-treated group（P 〈 0.05）. Conclusion SB203580 inhibits the expression of IL-1β and ICAM-1, and p38MAPK plays an important role in secondary tissues injury in perihematoma after ICH, possibly through the upregula- lion of inflammatory cytokines.