摘要
目的探讨一些药物对C反应蛋白(CRP)诱导脑微血管内皮细胞黏附分子表达的作用,为缺血性脑损伤机制及防治策略的进一步研究提供理论依据。方法培养脑微血管内皮细胞(bEnd.3),经辛伐他汀、吡格列酮、Hemin和AG490预处理后与CRP共孵育,采用免疫蛋白印迹(Western blotting)检测细胞黏附分子表达。结果CRP能显著诱导bEnd.3细胞表达细胞间黏附分子(ICAM-1)、血管细胞黏附分子(VCAM-1),信号转导子及转录激活子-3(STAT3)酪氨酸残基快速磷酸化。辛伐他汀、吡格列酮和AG490均能显著减少ICAM-1、VCAM-1的表达。结论CRP上调黏附分子表达的作用可能与JAK/STAT信号转导通路有关。辛伐他汀、吡格列酮均能抑制CRP诱导的脑内皮细胞ICAM-1、VCAM-1表达,可能是它们对缺血性脑损伤的保护机制之一。
Objective To determine possible effects of drugs on induction of cell adhesion molecules by C - reactive protein （CRP） in brain microvascular endothelium - derived cells （ bEnd. 3）. Methods Cultured bEnd. 3 cells were pretreated by simvastatin, pioglitazone, hemin and AG490 for 2 h, and then cells were stimulated with CRP （50 mg/L）. Expression of cell adhesion molecules was analyzed by Western blotting. Results CRP can induce significantly expressions of intercellular adhesion molecule （ ICAM - 1） and vascular cell adhesion molecule - 1 （VCAM - 1） （ P 〈0.01）, and stimulate rapidly phosphorylation of signal transducer and activator of transcription - 3 （STAT3） on tyrosine residues. Pretreatment with simvastatin, pioglitazone and AG490 can significantly reduce the inductions of adhesion molecules （ P 〈 0.05）. Conclusion Simvastatin or pioglitazone treatment decreased expression of adhesion molecules which would partly contribute to their protective effects on brain ischemic injury. The presentresults also indicated that JAK/STAT pathway might be involved in the induction of cell adhesion molecules by CRP.
出处
《中国微循环》
北大核心
2008年第4期219-221,231,共4页
Journal of Chinese Microcirculation
关键词
C反应蛋白
脑微血管内皮细胞
细胞黏附分子
C - reactive protein
Brain microvascular endothelial cells
Cell adhesion molecules
