摘要
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。
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 and Western blot respectively. Apoptosis index of lung was evaluated by TUNEL technique. The effect of SB203580, a p38MAPK inhibitor, on the apoptosis index of lung was observed. Results The expression of phospho-p38MAPK increased obviously after hyperoxia. Positive phospho-p38MAPK cells were mainly distributed in the alveolar, airway epithelial ceils, pulmonary vascular endothelium cells and infiltrative inflammatory cells. The apoptosis index of lung also significantly elevated. SB203580 inhibited the activation of p38MAPK, and reduced the apoptosis index of lung. Conclusions The phospho-p38MAPK increased and was expressed in many kinds of lung cells in lung injury rat model. It may play a role in the induction of apoptosis in hyperoxia-induced lung injury.
出处
《中国当代儿科杂志》
CAS
CSCD
北大核心
2009年第5期389-392,共4页
Chinese Journal of Contemporary Pediatrics
基金
国家自然科学基金资助项目(编号:30370618)
关键词
P38丝裂素活化蛋白激酶
高氧症
肺损伤
幼鼠
p38 mitogen-activated protein kinase
Hyperoxia
Lung injury
Juvenile rats
