Yahyapour Noushin, Eriksson Cecilia, Malmberg Per, Nygren Håkan
Department of Anatomy and Cell Biology, University of Gothenburg, P.O. Box 420, 405 30 Gothenburg, Sweden.
Biomaterials. 2004 Jul;25(16):3171-6. doi: 10.1016/j.biomaterials.2003.10.011.
Hydrophilic and hydrophobic titanium and glass were exposed to capillary whole blood between 5s and 24h. The time-sequence for adsorption of thrombin, kallikrein and complement C5b-9, and their relationship with adherent platelets and polymorphonuclear granulocyte (PMN) activation were investigated. Adsorbed thrombin and kallikrein were measured by cleavage of specific chromogenic substances, S-2238 and S-2303, respectively. Complement C5b-9 and expression of CD11b, CD66b, CD62P and Pan-platelets were measured by immunofluorescence. Thrombin and kallikrein were present on the surfaces during the whole investigated periods. Platelet adhesion and PMN cell adhesion and activation on all surfaces and activation of platelets on hydrophobic surfaces showed a similar pattern to thrombin adsorption. Kallikrein adsorption had a different pattern on each surface. C5b-9 was detected between 32min and 24h of blood exposure and a varying pattern of C5b-9 coverage was observed on each surface. In conclusion, our results indicate that the interaction between material and blood coagulation and kinin-activating proteins regulate the adhesion and activation of blood cells, whereas after longer time the coagulation and kallikrein-kinin system play minor roles and the complement system is decisive for mediating and elongating the inflammatory process.
将亲水性和疏水性钛及玻璃暴露于毛细血管全血中5秒至24小时。研究了凝血酶、激肽释放酶和补体C5b - 9的吸附时间序列，以及它们与黏附血小板和多形核粒细胞（PMN）活化的关系。吸附的凝血酶和激肽释放酶分别通过特异性显色物质S - 2238和S - 2303的裂解来测定。补体C5b - 9以及CD11b、CD66b、CD62P和全血小板的表达通过免疫荧光测定。在整个研究期间，表面均存在凝血酶和激肽释放酶。所有表面上的血小板黏附、PMN细胞黏附和活化以及疏水表面上的血小板活化均呈现出与凝血酶吸附相似的模式。激肽释放酶在每个表面上的吸附模式不同。在血液暴露32分钟至24小时之间检测到C5b - 9，并且在每个表面上观察到C5b - 9覆盖的不同模式。总之，我们的结果表明，材料与血液凝固和激肽激活蛋白之间的相互作用调节血细胞的黏附和活化，而在较长时间后，凝血和激肽释放酶 - 激肽系统起次要作用，补体系统对于介导和延长炎症过程起决定性作用。
