Activation of platelets upon contact with a vitamin E-coated/non-coated surface
Activation of platelets upon contact with a vitamin E-coated/non-coated surface
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DOI：
10.1007/s10047-013-0686-4
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发表时间：
2013-06-01
影响因子：
1.3
通讯作者：
Kobayashi, Hirosuke
中科院分区：
文献类型：
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作者：
Tsukao, Hiroshi;Kokubo, Kenichi;Kobayashi, Hirosuke
本研究的目的是确定维生素E涂层表面对血小板活化的影响，重点是维生素E涂层表面，血小板和白细胞之间的相互作用。使用富血小板血浆（PRP）或含白细胞的PRP（LPRP）。对于维生素E涂层膜，PRP和LPRP之间的血小板活化没有观察到差异，这意味着白细胞触发的血小板活化在与维生素E涂层膜接触的血浆中受到抑制，而膜本身直接诱导血小板活化。与PRP或LPRP接触的维生素E涂覆的膜的抗氧化能力部分降低，但仍有足够的残余能力。使用氧化维生素E涂覆的表面的体外实验显示，通过与氧化维生素E涂覆的表面接触诱导血小板中的P-选择素表达和超氧阴离子产生以及血小板粘附。我们的结论是，接触维生素E涂层的表面减少超氧阴离子介导的血小板活化，可能是通过减少超氧阴离子，但在减少的过程中，维生素E涂层的表面本身被氧化，这再次导致血小板活化。维生素E涂层透析器在血小板活化方面的有益作用被氧化维生素E的形成抵消。
The purpose of this study was to determine the effects of a vitamin E-coated surface on platelet activation, focusing on the interactions among the vitamin E-coated surface, platelets and leukocytes. Platelet-rich plasma (PRP) or PRP containing leukocytes (LPRP) was used. No difference was observed in platelet activation between PRP and LPRP for a vitamin E-coated membrane, meaning that platelet activation triggered by leukocytes was suppressed in plasma coming in contact with a vitamin E-coated membrane, while the membrane itself directly induced platelet activation. The antioxidant capacity of the vitamin E-coated membrane in contact with PRP or LPRP was partially reduced, but sufficient residual capacity remained. The in vitro experiments using an oxidized vitamin E-coated surface revealed that P-selectin expression and superoxide anion production in the platelets and platelet adhesion were induced by contact with the oxidized vitamin E-coated surface. We conclude that contact with a vitamin E-coated surface reduces platelet activation mediated by superoxide anions, probably by reducing superoxide anions, but during the process of the reduction, the vitamin E-coated surface itself becomes oxidized, which again causes platelet activation. The beneficial effects of a vitamin E-coated dialyzer in respect of platelet activation were counteracted by the formation of oxidized vitamin E.