中文摘要：

目的观察p38MAPK特异性抑制剂SB203580对缺氧致人脐静脉内皮细胞（Human umbilical vein endothelial cells,HUVECs）损伤的保护作用。方法将HUVECs分为正常对照组、缺氧培养组、SB203580＋正常对照组和SB203580＋缺氧培养组,培养24h后,流式细胞术检测各组细胞的凋亡率;Western blot分析各组细胞p38MAPK蛋白及其磷酸化水平;Transwell小室模型检测各组细胞的迁移率;ELISA法检测各组细胞培养上清中可溶性血管内皮生长因子受体-1（sFlt-1）及可溶性Endoglin（sEng）的含量。结果与正常对照组相比,缺氧培养组细胞的凋亡率、p38MAPK的磷酸化水平、sFlt-1及sEng含量显著增加（P〈0.01）,细胞体外迁移能力下降;SB203580＋缺氧培养组细胞的凋亡率、p38MAPK的磷酸化水平、sFlt-1和sEng的释放较缺氧培养组均下降,体外迁移能力增强（P〈0.05）;磷酸化p38MAPK的释放水平与sFlt-1及sEng含量呈正相关（r1=0.69,P〈0.05;r2=0.71,P〈0.05）。结论 SB203580通过特异性阻断p38MAPK信号转导通路,对缺氧培养的HUVECs产生保护作用。

英文摘要：

Objective To observe the protective effect of SB203580,a specific inhibitor of p38 MAPK,on the injury of human umbilical vein endothelial cells（HUVECs）induced by hypoxia.Methods HUVECs were divided into normal control,hypoxia,SB203580 ＋ normal control and SB203580 ＋ hypoxia groups,cultured for 24 h,then determined for apoptosis rate by flow cytometry,for p38 MAPK protein and its phosphorylation level by Western blot,for migration rate by Transwell test,and for soluble vascular endothelial growth factor receptor-1（sFlt-1）and soluble Endoglin（sEng）contents in culture supernatant by ELISA.Results Compared with those in normal control group,the cell apoptosis rate,phosphorylation level of p38 MAPK as well as sFlt-1 and sEng contents in hypoxia group increased significantly（P 0.01）,while the in vitro migration ability of cells decreased.However,compared with those in hypoxia group,the cell apoptosis rate,phosphorylation level of p38 MAPK as well as release of sFlt-1 and sEng in SB203580 ＋ hypoxia group decreased,while the in vitro migration ability of cells increased（P 0.05）.The release level of phosphorylated p38 MAPK was positively related to the sFlt-1 and sEng contents（r1 = 0.69,P 0.05;r2 = 0.71,P 0.05）.Conclusions SB203580 showed protective effect on HUVECs cultured under condition of hypoxia by specifically blocking the signal transduction pathway of p38 MAPK.