摘要
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。
Objective To study the role of p38 mitogen-activated protein kinase (MAPK) in lipopolysaccharide (LPS) induced expression of intercellular adhesion molecule-1 (ICAM-1) on human umbilical vein endothelial cell (HUVEC) Methods HUVEC was harvested and cultured before being divided into two groups,i,e.stimulating group(S) and priming group(P). In S group, the cultured endothelial cell was stimulated by LPS.In P group,endothelial cell was pre-treated with SB 203580 2 hours before LPS stimulation. The expressions of ICAM-1 mRNA and protein in HUVEC of two groups and their dose-effect relationship with stimulator and inhibitor were observed.Furthermore the p38 mRNA activity of HUVEC was detected, Results After LPS stimulation,ICAM-1 molecule on the surface of endothelium increased significantly at 8 to 36 hours. Cytoplasmic mRNA increased obviously at 2 hours.The activity of p38 MAPK increased at 15 min and reached peak value at 30 to 60 min after that HUVEC was stimulated by LPS. Conclusion Inhibitor SB 203580 of p38 might significantly inhibit the inducing effect of LPS .LPS could regulate the expression of ICAM-1 gene and protein in HUVEC by activating p38 MAPK signal transduction passage.
出处
《中华烧伤杂志》
CAS
CSCD
2001年第1期32-35,共4页
Chinese Journal of Burns
基金
国家自然科学基金重点资助项目!(39830400)
