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多形核白细胞对肝素辅因子II的灭活作用。

Inactivation of heparin cofactor II by polymorphonuclear leukocytes.

作者信息

Sie P, Dupouy D, Dol F, Boneu B

机构信息

Laboratoire d'Hémostase, Centre de Transfusion Sanguine, Toulouse, France.

出版信息

Thromb Res. 1987 Sep 15;47(6):657-64. doi: 10.1016/0049-3848(87)90104-6.

Abstract

Inactivation of purified human heparin cofactor II by polymorphonuclear leukocytes was investigated. A proteolytic mechanism of inactivation was demonstrated by SDS-polyacrylamide gel electrophoresis. Inactivation and related proteolysis did not occur in the presence of unstimulated leukocytes and were prevented by various protease inhibitors. Heparin cofactor II was inactivated more rapidly than antithrombin III. However, heparin (1-10 ug/ml) strongly accelerated the rate of antithrombin III inactivation and slightly protected heparin cofactor II, thus reversing the order of inactivation. Dermatan sulfate had no effect on this process.

摘要

研究了多形核白细胞对纯化的人肝素辅因子II的灭活作用。通过SDS-聚丙烯酰胺凝胶电泳证明了一种蛋白水解失活机制。在未刺激的白细胞存在下,不会发生失活和相关的蛋白水解,并且各种蛋白酶抑制剂可阻止这种情况发生。肝素辅因子II的失活速度比抗凝血酶III更快。然而,肝素(1-10微克/毫升)强烈加速了抗凝血酶III的失活速度,并对肝素辅因子II有轻微保护作用,从而逆转了失活顺序。硫酸皮肤素对这一过程没有影响。

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