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目的 研究p38丝裂原激活蛋白激酶（MAPK）信号转导通路在脂多糖（LPS）诱导人脐静脉内皮细胞（HUVEC）表达细胞间粘附分子-1（ICAM-1）中的作用。 方法 脐静脉内皮细胞培养后分为两组：（1）刺激组，设不同时相点分别用LPS刺激内皮细胞；（2）预处理组，在LPS刺激前2 h，用SB203580预处理内皮细胞。观察ICAM-1蛋白和mRNA表达的变化，检测内皮细胞p38 MAPK活性变化。 结果 LPS剌激后，内皮细胞表面ICAM-1分子在8～36 h显著增加，胞浆中mRNA在2 h即有显著增加；LPS刺激HUVEC后15 min，p38 MAPK 活性即有升高，30～60 min达高峰。p38抑制剂SB203580可显著抑制LPS的诱导作用。 结论 LPS 可能通过激活p38 MAPK信号转导通路，调节HUVEC的ICAM-1基因和蛋白表达。
AIM To investigate the role of MAPK signal transduction pathway in the expression of intercellular adhesion molecule-1 (ICAM-1) induced by lipopolysaccharide (LPS) in human umbilical vein endothelial cells (HUVECs). Methods Umbilical vein endothelial cells were cultured and divided into two groups: (1) stimulation group, which were stimulated with LPS at different time points; (2) pretreatment group, 2 h before LPS stimulation, SB203580 pretreated endothelial cells . The changes of ICAM-1 protein and mRNA expression were observed to detect the changes of p38 MAPK activity in endothelial cells. Results After stimulated with LPS, ICAM-1 molecules on the surface of endothelial cells increased significantly from 8 to 36 h, mRNA in cytoplasm increased significantly at 2 h. After LPS stimulation for 15 min, the activity of p38 MAPK increased, 60 min reached the peak. p38 inhibitor SB203580 can significantly inhibit the induction of LPS. Conclusion LPS may regulate ICAM-1 gene and protein expression in HUVEC by activating the p38 MAPK signal transduction pathway.