Ehrlich Daniela, Humpel Christian
Laboratory of Psychiatry and Exp. Alzheimer's Research, Department of Psychiatry and Psychotherapy, Innsbruck Medical University , Innsbruck , Austria.
Platelets. 2014;25(1):16-22. doi: 10.3109/09537104.2013.764979. Epub 2013 Feb 12.
It is known that oxidative stress leads to amyloid precursor protein (APP) dysregulation in platelets. Ethanol (EtOH) is a vascular risk factor and induces oxidative stress. The aim of the present study was thus to investigate whether EtOH affects APP processing in rat and human platelets. Platelets were exposed to 50 mM EtOH with and without 2 mM calcium-chloride (CaCl₂) for 20 or 180 minutes at 37°C. Platelet aggregation, serotonin release and APP isoforms 130 and 106/110 kDa were analyzed. As a control, 100 mM H₂O₂ was tested in rat platelets. Our data show that EtOH alone did not affect any of the analyzed parameters, whereas CaCl₂ significantly increased aggregation of rat and human platelets. In addition, CaCl₂ alone enhanced serotonin release in rat platelets. EtOH counteracted CaCl₂-induced aggregation and serotonin release. In the presence of CaCl₂, EtOH reduced the 130 kDa APP isoform in rat and human platelets. In conclusion, this study shows that in the presence of CaCl₂, EtOH affects the platelet function and APP processing in rat and human platelets.
已知氧化应激会导致血小板中淀粉样前体蛋白（APP）失调。乙醇（EtOH）是一种血管危险因素，可诱导氧化应激。因此，本研究的目的是调查EtOH是否会影响大鼠和人类血小板中APP的加工过程。将血小板在37°C下分别暴露于含有和不含有2 mM氯化钙（CaCl₂）的50 mM EtOH中20或180分钟。分析血小板聚集、5-羟色胺释放以及APP的130 kDa和106/110 kDa亚型。作为对照，在大鼠血小板中测试了100 mM过氧化氢（H₂O₂）。我们的数据表明，单独的EtOH不会影响任何分析参数，而CaCl₂会显著增加大鼠和人类血小板的聚集。此外，单独的CaCl₂会增强大鼠血小板中的5-羟色胺释放。EtOH可抵消CaCl₂诱导的聚集和5-羟色胺释放。在存在CaCl₂的情况下，EtOH会降低大鼠和人类血小板中130 kDa的APP亚型。总之，本研究表明，在存在CaCl₂的情况下，EtOH会影响大鼠和人类血小板的功能以及APP的加工过程。
