摘要
F-MLP与白三烯B_4能增加中性多形核白细胞(PMNL)对人脐静脉内皮细胞的粘附率。白三烯B_4处理的PMNL刺激内皮细胞产生6-酮-PGF_1a,F-MLP或自三烯B_4处理的PMNL促进内皮细胞释放von Willebrand因子。眼镜蛇毒抑制F-MLP或白三烯B_4对PMNL粘附的刺激作用,但这种PMNL仍能促进内皮细胞的花生四烯酸代谢与von Willebrand因子释放。而用F-MLP、白三烯B_4和/或眼镜蛇毒预先处理内皮细胞,不影响白细胞的粘附,也不影响内皮细胞释放6-酮-PGF_1a与von Willebrand因子。这些体外试验结果表明,F-MLP与白三烯B_4在刺激PMNL-内皮细胞粘附中主要的靶细胞是PMNL而不是内皮细胞。PMNL在没有粘附于内皮细胞的情况下也可能通过释放某些介质影响内皮细胞的功能。
F-MLP and LTB. augmented PMNL in vitro adherence to human umbilical vein endothelial cell (HUVE) monolayers. The LTB_4-treated PMNL stimulated endothelial cell 6-keto-PGF_1α formation. F-MLP-or LTB_4-treatcd PMNL promoted the release of vWF from endothelial cells. PMNL adherence stimulated by F-MLP or LTB, was inhibited significantly by preincubation with cobra venom, but such PMNL maintained their ability to promote eicosanoid metabolism in HUVE and also vWF release from HUVE. On the contrary, incubation of HUVE monolayers with F-MLP, LTB, and/or cobra venom did not modify either PMNL, for subsequent adhesion or endothelial cell for vWF/6-keto-PGF_1α release. Our results suggested that the principal target of F-MLP and LTB, in stimulating PMNL-endothelial cell adherence is PMNL rather than endothelial cells. PMNL can also act on endothelial cells probably in the ways of producing some mediators, even if no adherence occurs.
出处
《中国病理生理杂志》
CAS
CSCD
北大核心
1991年第5期550-553,共4页
Chinese Journal of Pathophysiology
关键词
白细胞
内皮细胞
蛇毒
Endothelium
Neutpophils Leukotrienes B
Snake venoms
6-keto-prostaglandin F_1 alpha
