慢性低氧对肺动脉高压大鼠肺血管ERK 1/2、p38MAPK表达的影响

目的：通过建立慢性低氧性肺动脉高压大鼠模型,研究慢性低氧对大鼠肺血管细胞外信号调节蛋白激酶(ERK1/2)、p38MAPK蛋白表达的影响。方法建立慢性常压低氧肺动脉高压大鼠模型,将雄性SD大鼠随机分为正常对照组、低氧1d、3d、7d、14d和21d组,应用免疫组织化学技术检测肺动脉高压形成过程中大鼠肺血管 ERK1/2、p38MAPK 蛋白表达水平。结果①RVSP 和 RV/(LV+S)比值较正常对照组明显增加(P<0.05),低氧后3 d、7 d、14 d和21 d后大鼠肺血管明显增厚；②ERK1/2、p38MAPK蛋白广泛分布于肺血管内皮细胞、平滑肌细胞和成纤维细胞中,且随着低氧时间的延长,ERK1/2、p38MAPK蛋白表达量增加。结论 ERK1/2、p38MAPK 蛋白表达量的上调可能参与了慢性低氧诱导的大鼠肺动脉高压肺血管重塑的发生、发展过程。

Changes of ERK1/2,p38MAPK in pulmonary vascular remodeling of chronic hypoxia-induced rat pulmonary ;hypertension

Objective In this study,with hypoxia-induced pulmonary hypertension rats model,to investigate the expression variation of ERK1/2,p38MAPK in rat pulmonary arteries.Methods Establish the rat model of pulmonary hypertension with sixty male SD rats which were randomly divided into a normal control group,hypoxic exposure 1 day,3 days,7 days,1 4 days and 2 1 days groups and with 1 0 rats in each group.The expression of ERK1/2,p38MAPK protein in rat pulmonary arteries of each group was detected by immunohistochemistry.Results ①RVSP and RV/(LV+S) increased significantly than normal control groups (P<0.05),rats pulmonary vascular thicking after chronic hypoxia 3 d,7 d,14 d,and 21 d.②ERK1/2, p38MAPK protein were widely distributed in pulmonary arterial endothelial cells,smooth muscle cells and fibroblasts.And the longer of the time of hypoxic exposure,the more of protein expression.Conclusions ERK1/2,p38MAPK protein expression is involved in the development of pulmonary vascular remodeling of chronic hypoxic-induced rat PH.