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己酮可可碱对内毒素激活的单核细胞产生的促凝血活性的抑制作用

[Inhibition by pentoxifylline of procoagulant activity produced by endotoxin-active monocytes].

作者信息

de Prost D, Ollivier V, Hakim J

机构信息

Laboratoire d'immunologie et d'hématologie, U INSERM 294, CHU Xavier Bichat, Paris.

出版信息

C R Seances Soc Biol Fil. 1992;186(3):186-92.

PMID:1283564
Abstract

When appropriately stimulated, monocytes are able to initiate blood coagulation through the membrane expression of tissue factor. This procoagulant activity is thought to play a role in activating coagulation in response to inflammatory stimuli in vivo. We found that pentoxifylline, a methylxanthine derivative already reported to regulate some monocyte functions, inhibits the procoagulant activity developed by monocytes in vitro in response to endotoxin. This effect was accompanied by an early increase in intracellular levels of cyclic AMP and was mimicked by compounds that induce an increase in cyclic AMP levels. These results suggest that the suppressive effect of pentoxifylline occurs at least in part via an increase in intracellular cyclic AMP levels.

摘要

受到适当刺激时,单核细胞能够通过组织因子的膜表达启动血液凝固。这种促凝活性被认为在体内对炎症刺激作出反应时激活凝血过程中发挥作用。我们发现,已报道可调节某些单核细胞功能的甲基黄嘌呤衍生物己酮可可碱,能抑制单核细胞在体外对内毒素产生的促凝活性。这一效应伴随着细胞内环磷酸腺苷(cAMP)水平的早期升高,并且可诱导cAMP水平升高的化合物也能模拟这一效应。这些结果表明,己酮可可碱的抑制作用至少部分是通过细胞内cAMP水平升高实现的。

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