p38丝裂素活化蛋白激酶在幼鼠高氧肺损伤模型中的表达及作用

目的：近年来的研究证实p38丝裂素活化蛋白激酶（p38MAPK）在多种因素诱导的肺损伤中发挥着重要的调控作用，但其在高氧肺损伤中的表达和作用尚不明了。该文通过建立幼鼠高氧肺损伤模型来研究p38MAPK在该模型中的表达及作用。方法：90％氧气暴露建立幼年Wistar大鼠高氧肺损伤模型，用免疫组化和蛋白质免疫印迹法观察p38MAPK在肺组织中的分布和表达，用TUNEL法观察肺组织的细胞凋亡指数，并同时观察p38MAPK抑制剂SB203580对肺组织细胞凋亡的影响。结果：高氧暴露后肺组织磷酸化p38MAPK蛋白表达明显增强，主要分布于肺泡上皮细胞、气道上皮细胞、血管内皮细胞、浸润炎症细胞。同时肺凋亡指数明显增加。使用SB203580抑制了p38MAPK活性的上升，同时降低了肺凋亡指数。结论：高氧诱导的急性肺损伤模型中，磷酸化的p38MAPK表达增加，并表达于肺内多种细胞，可能起促凋亡作用。［中国当代儿科杂志，2009，11（5）：389-392］

Expression and role of p38 mitogen-activated protein kinase in hyperoxia-induced lung injury juvenile rat model

Objective Some research has shown that p38 mitogen-activated protein kinase (p38MAPK) plays important roles in lung injuries induced by various factors. Its expression and role in hyperoxia-induced lung injury remains unknown. This study investigated the expression and role of p38MAPK in hyperoxia-induced lung injury juvenile rat model.Methods Hyperoxia-induced lung injury rat model was prepared by 90% O2 exposure. The location and expression of p38MAPK in lung tissues were detected by immunohistochemistry ...