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活化蛋白C(APC)在抑制炎症反应中起着重要作用,内皮细胞蛋白C受体(EPCR)可以增加蛋白C的活化。已有的研究表明:APC通过抑制细胞因子和化学趋化因子的分泌以及黏附分子的表达来调节炎症反应,但其作用机制还不完全明了。本文研究了APC对TNF-α诱导的细胞因子分泌和黏附分子表达的影响,同时探讨了其可能的作用机制。结果显示:APC能显著抑制TNF-α诱导的细胞因子分泌(IL-1α和IL-8)和黏附分子表达(ICAM-1,VCAM-1 and E-selction);抗EPCR的单克隆抗体显著拮抗了APC抑制细胞因子分泌和黏附分子表达的功能。结论:APC通过抑制炎症因子的产生来调节炎症反应,这种作用可能是通过与内皮细胞EPCR的相互作用来实现。
Activated protein C (APC) plays an important role in the suppression of inflammatory reactions, and endothelial cell protein C receptor (EPCR) increases protein C activation. Some researches have shown that APC regulates the inflammatory response by inhibiting the secretion of cytokines and chemokines and the expression of adhesion molecules, but its mechanism of action is not completely understood. In this paper, the effects of APC on the secretion of cytokines and the expression of adhesion molecules induced by TNF-αwere studied. At the same time, the possible mechanism was explored. The results showed that APC significantly inhibited TNF-α-induced cytokine secretion (IL-1α and IL-8) and adhesion molecule expression (ICAM-1, VCAM-1 and E-selction); anti-EPCR monoclonal antibody was significantly antagonized APC inhibits cytokine secretion and adhesion molecule expression. Conclusion: APC regulates the inflammatory response by inhibiting the production of inflammatory cytokines, which may be through the interaction with endothelial cells EPCR.