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Eugenol Suppresses Platelet Activation and Mitigates Pulmonary Thromboembolism in Humans and Murine Models.
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- المؤلفون: Huang, Wei-Chieh1 (AUTHOR) ; Shu, Lan-Hsin2 (AUTHOR); Kuo, Yu-Ju1 (AUTHOR); Lai, Kevin Shu-Leung3 (AUTHOR); Hsia, Chih-Wei4 (AUTHOR); Yen, Ting-Lin5 (AUTHOR); Hsia, Chih-Hsuan6 (AUTHOR); Jayakumar, Thanasekaran7 (AUTHOR) ; Yang, Chih-Hao8 (AUTHOR) ; Sheu, Joen-Rong1,8 (AUTHOR)
- المصدر:
International Journal of Molecular Sciences. Feb2024, Vol. 25 Issue 4, p2098. 16p.
- الموضوع:
- معلومة اضافية
- نبذة مختصرة :
Platelets assume a pivotal role in the pathogenesis of cardiovascular diseases (CVDs), emphasizing their significance in disease progression. Consequently, addressing CVDs necessitates a targeted approach focused on mitigating platelet activation. Eugenol, predominantly derived from clove oil, is recognized for its antibacterial, anticancer, and anti-inflammatory properties, rendering it a valuable medicinal agent. This investigation delves into the intricate mechanisms through which eugenol influences human platelets. At a low concentration of 2 μM, eugenol demonstrates inhibition of collagen and arachidonic acid (AA)-induced platelet aggregation. Notably, thrombin and U46619 remain unaffected by eugenol. Its modulatory effects extend to ATP release, P-selectin expression, and intracellular calcium levels ([Ca2+]i). Eugenol significantly inhibits various signaling cascades, including phospholipase Cγ2 (PLCγ2)/protein kinase C (PKC), phosphoinositide 3-kinase/Akt/glycogen synthase kinase-3β, mitogen-activated protein kinases, and cytosolic phospholipase A2 (cPLA2)/thromboxane A2 (TxA2) formation induced by collagen. Eugenol selectively inhibited cPLA2/TxA2 phosphorylation induced by AA, not affecting p38 MAPK. In ADP-treated mice, eugenol reduced occluded lung vessels by platelet thrombi without extending bleeding time. In conclusion, eugenol exerts a potent inhibitory effect on platelet activation, achieved through the inhibition of the PLCγ2–PKC and cPLA2-TxA2 cascade, consequently suppressing platelet aggregation. These findings underscore the potential therapeutic applications of eugenol in CVDs. [ABSTRACT FROM AUTHOR]
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