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http://ir.cmu.edu.tw/ir/handle/310903500/30515
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| 題名: | Gene frequencies of the HPA-1 to HPA-8w platelet antigen alleles in Taiwanese, Indonesian, and Thai |
| 作者: | Liu, TC;Shih, MC;Lin, CL;Lin, SF;Chen, CM;Chang, JG |
| 貢獻者: | 附設醫院醫研部;China Med Coll Hosp, Dept Lab Med, Taichung, Taiwan;China Med Coll Hosp, Dept Med Res, Taichung, Taiwan;Kaohsiung Med Univ Hosp, Div Hematooncol, Dept Med, Kaohsiung, Taiwan |
| 日期: | 2002 |
| 上傳時間: | 2010-09-24 14:56:51 (UTC+8) |
| 出版者: | SPRINGER-VERLAG |
| 摘要: | In the present study, the antiplatelet effect and its mechanism of a new synthetic compound YD-3 [1-benzyl-3-(ethoxycarbonylphenyl)indazole] were examined. YD-3 inhibited the aggregation of washed human platelets caused by protease-activated receptor (PAR) 4 agonist peptide GYPGKF (IC50 = 0.13 +/- 0.02 muM), but had no or little effect on that by thrombin, PAR1 agonist peptide SFLLRN, collagen or U46619. YD-3 produced a parallel, rightward shift of the concentration-response curve for GYPGKF without decreasing of the maximum platelet aggregation, indicating a competitive antagonism. In contrast to human platelets, both thrombin- and GYPGKF-induced mouse platelet shape change and aggregation were completely inhibited by YD-3. YD-3 also selectively prevented GYPGKF-induced intracellular Ca2+ mobilization in human platelets. Furthermore, in the PAR1-desensitized human platelets. thrombin induced a relatively slow rise and decay of calcium mobilization that was significantly inhibited by YD-3. In addition, the synergistic effect of SFLLRN and GYPGKF on platelet activation was prevented by YD-3. YD-3 also inhibits both fMLP-stimulated neutrophil- and purified cathepsin G-induced platelet aggregation, which has been demonstrated to be PAR4-dependent. Taken together, our results suggest that YD-3 selectively inhibits PAR4-dependent platelet activation through blockade of PAR4. To the best of our knowledge, it is the first non-peptide PAR4 antagonist. |
| 關聯: | ANNALS OF HEMATOLOGY 81(5):244-248 |
| 顯示於類別: | [台中附設醫院] 期刊論文
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