新生鼠高氧肺损伤中p38MAPK的磷酸化

目的 探讨p38丝裂素活化蛋白激酶(p38 mitogen-activated protein kinase,p38MAPK)在新生鼠高氧肺损伤中的表达及意义.方法 160只新生鼠分为空气对照组、高氧肺损伤组、高氧肺损伤 SB203580组和高氧肺损伤 生理盐水组,分别建立动物模型.在12、24、72 h和1周4个时相点处死,进行肺组织病理学检查、肺湿/干重比值(W/D)测定、Western blot法检测p38MAPK的表达.结果 高氧暴露72 h即可建立肺损伤模型.新生鼠暴露于高氧12h后,p38MAPK开始表达,72h达高峰,后逐渐降低.在高氧暴露72 h后,空气对照组未见p38MAPK表达,高氧肺损伤组可见p38MAPK表达;高氧肺损伤 生理盐水组p38MAPK表达明显强于高氧肺损伤 SB203580组.结论 p38MAPK参与了新生鼠高氧肺损伤的过程,SB203580可以减轻这种损伤.

Phosphorylation of p38MAPK in hyperoxia-induced lung injury of new-born rats

Objective To investigate the expression and significance of p38 mitogen-activated protein kinase (p38MAPK) in hyperoxia-induced lung injury of new-born rats. Methods Totally 160 rats at the age of 12 h were randomly and equally divided into air control group, hyperoxia-induced lung injury group, hyperoxia-induced lung injury SB203580 group and hyperoxia-induced lung injury normal saline group. After the injury was inflicted, SB203580 or normal saline at same volume was given intraperitoneally at 5 mg/kg. After the rats were executed at the time points of 12, 24, 72 h and 1 week after the model establishment, the right upper lungs were resected for histopathology, right below lungs for wet weight/dry weight, and left lungs for detecting the expression of p38MAPK by Western blot analysis. Results Hyperoxia-induced lung injury model were established successfully after 72 h by exposure to hyperoxia. No p38MAPK expression was observed in air control group. In hyperoxia-induced lung injury group p38MAPK was detected from 12 h, reached to the peak at 72 h, and decreased 1 week later, and its expression was significantly higher in this group and normal saline group than in SB203580 group. Conclusion p38MAPK is involved in the process of hyperoxia-induced lung injury, and the injury can be relieved by treatment of SB203580.