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Int. J. Mol. Sci. 2017, 18(7), 1500; doi:10.3390/ijms18071500

Licochalcone A Prevents Platelet Activation and Thrombus Formation through the Inhibition of PLCγ2-PKC, Akt, and MAPK Pathways

1
School of Medicine, College of Medicine, Taipei Medical University, Taipei 110, Taiwan
2
Department of Neurology, Shin Kong Wu Ho Su Memorial Hospital, Taipei 111, Taiwan
3
Department of Pharmacology and Graduate Institute of Medical Sciences, Taipei Medical University, Taipei 110, Taiwan
4
Central Laboratory, Shin Kong Wu Ho Su Memorial Hospital, Taipei 111, Taiwan
5
Department of Medical Research and Division of General Surgery, Department of Surgery, Taipei Medical University Hospital, Taipei 110, Taiwan
6
College of Medicine, Fu-Jen Catholic University, Taipei 242, Taiwan
7
Graduate Institute of Metabolism and Obesity Sciences, College of Public Health and Nutrition, Taipei Medical University, Taipei 110, Taiwan
These authors contributed equally to this work.
*
Authors to whom correspondence should be addressed.
Received: 5 June 2017 / Revised: 7 July 2017 / Accepted: 9 July 2017 / Published: 12 July 2017
(This article belongs to the Special Issue Molecular Pharmacology and Pathology of Strokes)
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Abstract

Platelet activation is involved in cardiovascular diseases, such as atherosclerosis and ischemic stroke. Licochalcone A (LA), an active ingredient of licorice, exhibits multiple biological activities such as anti-oxidation and anti-inflammation. However, its role in platelet activation remains unclear. Therefore, the study investigated the antiplatelet mechanism of LA. Our data revealed that LA (2–10 μM) concentration dependently inhibited platelet aggregation induced by collagen, but not thrombin and U46619. LA markedly attenuated collagen-stimulated ATP release, P-selectin secretion, calcium mobilization, and GPIIbIIIa activation, but did not interfere with the collagen binding to platelets. Moreover, LA significantly reduced the activation of PLCγ2, PKC, Akt and MAPKs. Thus, LA attenuates platelet activation, possibly by inhibiting collagen receptor downstream signaling but not by blocking the collagen receptors. In addition, LA prevented adenosine diphosphate (ADP)-induced acute pulmonary thrombosis, fluorescein sodium-induced platelet thrombus formation, and middle cerebral artery occlusion/reperfusion-induced brain injury in mice, but did not affect normal hemostasis. This study demonstrated that LA effectively reduced platelet activation and thrombus formation, in part, through the inhibition of PLCγ2–PKC, Akt, and MAPK pathways, without the side effect of bleeding. These findings also indicate that LA may provide a safe and alternative therapeutic approach for preventing thromboembolic disorders such as stroke. View Full-Text
Keywords: Licochalcone A; middle cerebral artery occlusion; platelet activation; PLCγ2–PKC; thrombus formation Licochalcone A; middle cerebral artery occlusion; platelet activation; PLCγ2–PKC; thrombus formation
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MDPI and ACS Style

Lien, L.-M.; Lin, K.-H.; Huang, L.-T.; Tseng, M.-F.; Chiu, H.-C.; Chen, R.-J.; Lu, W.-J. Licochalcone A Prevents Platelet Activation and Thrombus Formation through the Inhibition of PLCγ2-PKC, Akt, and MAPK Pathways. Int. J. Mol. Sci. 2017, 18, 1500.

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