ArticleInternational journal of molecular sciences2017
Licochalcone A Prevents Platelet Activation and Thrombus Formation through the Inhibition of PLCγ2-PKC, Akt, and MAPK Pathways.
Article in International journal of molecular sciences, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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23 citing papers in PubMed, 57 citations in OpenAlex.
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- A novel naphthalimide derivative reduces platelet activation and thrombus formation via suppressing GPVI.Journal of cellular and molecular medicine · 2021Article
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- Phospholipase D1 and D2 Synergistically Regulate Thrombus Formation.International journal of molecular sciences · 2020Article
- Inhibition of human thrombin by the constituents of licorice: inhibition kinetics and mechanistic insights throughRSC advances · 2020Article
- Network Pharmacology-Based Approach Uncovers the Mechanism of GuanXinNing Tablet for Treating Thrombus by MAPKs Signal Pathway.Frontiers in pharmacology · 2020Article
- Effect of Huoxiang Zhengqi Pill on Early Neurological Deterioration in Patients with Acute Ischemic Stroke Undergoing Recanalization Therapy and Predictive Effect of Essen Score.Evidence-based complementary and alternative medicine : eCAM · 2020Article
- VAS2870 and VAS3947 attenuate platelet activation and thrombus formation via a NOX-independent pathway downstream of PKC.Scientific reports · 2019Article
- Embelin as a Novel Inhibitor of PKC in the Prevention of Platelet Activation and Thrombus Formation.Journal of clinical medicine · 2019Article
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
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.
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