Furukawa K I, Matsuzawa M, Tsurufuji S, Watanabe K, Ohizumi Y
Department of Pharmaceutical Molecular Biology, Faculty of Pharmaceutical Sciences, Tohoku University, Sendai, Japan.
Jpn J Pharmacol. 1997 Nov;75(3):295-8.
2,5-Di-(tert-butyl)-1,4-benzohydroquinone (tBuBHQ), an inhibitor of endoplasmic reticulum Ca2+-ATPase, caused aggregation accompanied by a marked increase in intracellular Ca2+ concentrations ([Ca2+]i) in washed rabbit platelets. Treatment of platelets with SK&F96365 or removal of extracellular Ca2+ inhibited both Ca2+ influx and platelet aggregation induced by tBuBHQ. These responses of platelets to tBuBHQ were also inhibited by genistein. Western blots using antibody against phosphorylated amino acid residues revealed that tBuBHQ activated tyrosine kinase independently of extracellular Ca2+. These results suggest that tBuBHQ induces Ca2+ influx into platelets probably through activation of tyrosine kinase, resulting in platelet aggregation.
2,5-二-（叔丁基）-1,4-苯并氢醌（tBuBHQ）是一种内质网Ca2 + -ATP酶抑制剂，它会导致洗涤过的兔血小板发生聚集，并伴随着细胞内Ca2 +浓度（[Ca2 +] i）显著升高。用SK&F96365处理血小板或去除细胞外Ca2 +可抑制tBuBHQ诱导的Ca2 +内流和血小板聚集。血小板对tBuBHQ的这些反应也受到金雀异黄素的抑制。使用针对磷酸化氨基酸残基的抗体进行的蛋白质免疫印迹显示，tBuBHQ可独立于细胞外Ca2 +激活酪氨酸激酶。这些结果表明，tBuBHQ可能通过激活酪氨酸激酶诱导Ca2 +流入血小板，从而导致血小板聚集。
