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| 題名: | Antipsychotic Drugs Inhibit Platelet Aggregation via P2Y(1) and P2Y(12) Receptors |
| 作者: | Wu, CC (Wu, Chang-Chieh)
Tsai, FM (Tsai, Fu-Ming)
Chen, ML (Chen, Mao-Liang)
Wu, S (Wu, Semon)
Lee, MC (Lee, Ming-Cheng)
Tsai, TC (Tsai, Tzung-Chieh)
Wang, LK (Wang, Lu-Kai)
Wang, CH (Wang, Chun-Hua) |
| 貢獻者: | 生科系 |
| 關鍵詞: | SCHIZOPHRENIC-PATIENTS
ATYPICAL ANTIPSYCHOTICS
CLINICAL-RESPONSE
ADP RECEPTORS
TNF-ALPHA
RISPERIDONE
DIFFERENTIATION
HALOPERIDOL
PATHWAY
BIOGENESIS |
| 日期: | 2016 |
| 上傳時間: | 2017-04-18 09:46:33 (UTC+8) |
| 摘要: | Antipsychotic drugs (APDs) used to treat clinical psychotic syndromes cause a variety of blood dyscrasias. APDs suppress the aggregation of platelets; however, the underlying mechanism remains unknown. We first analyzed platelet aggregation and clot formation in platelets treated with APDs, risperidone, clozapine, or haloperidol, using an aggregometer and rotational thromboelastometry (ROTEM). Our data indicated that platelet aggregation was inhibited, that clot formation time was increased, and that clot firmness was decreased in platelets pretreated with APDs. We also examined the role two major adenosine diphosphate (ADP) receptors, P2Y(1) and P2Y(12), play in ADP-mediated platelet activation and APD-mediated suppression of platelet aggregation. Our results show that P2Y(1) receptor stimulation with ADP-induced calcium influx was inhibited by APDs in human and rats' platelets, as assessed by in vitro or ex vivo approach, respectively. In contrast, APDs, risperidone and clozapine, alleviated P2Y(12)-mediated cAMP suppression, and the release of thromboxane A2 and arachidonic acid by activated platelets decreased after APD treatment in human and rats' platelets. Our data demonstrate that each APD tested significantly suppressed platelet aggregation via different mechanisms. |
| 關聯: | BIOMED RESEARCH INTERNATIONAL 文獻號碼: 2532371 |
| 顯示於類別: | [生命科學系] 期刊論文
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