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霍诺醇作为人血小板胶原受体糖蛋白 VI 的特异性拮抗剂：功能的在体和体内研究。

Honokiol as a specific collagen receptor glycoprotein VI antagonist on human platelets: Functional ex vivo and in vivo studies.

机构信息

Graduate Institute of Medical Sciences and Department of Pharmacology, College of Medicine, Taipei Medical University, Taipei, Taiwan.

Division of Cardiology, Department of Internal Medicine, Cathay General Hospital, Taipei, Taiwan.

出版信息

Sci Rep. 2017 Jan 5;7:40002. doi: 10.1038/srep40002.

DOI:10.1038/srep40002
PMID:28054640
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5213647/
Abstract

Honokiol, derived from Magnolia officinalis, has various pharmacological properties. Platelet activation plays a critical role in cardiovascular diseases. Honokiol has been reported to inhibit collagen-stimulated rabbit platelet aggregation. However, detailed further studies on the characteristics and functional activity of honokiol in platelet activation are relatively lacking. In the present study, honokiol specifically inhibited platelet aggregation and Ca ion mobilization stimulated with collagen or convulxin, an agonist of glycoprotein (GP) VI, but not with aggretin, an agonist of integrin αβ. Honokiol also attenuated the phosphorylation of Lyn, PLCγ2, PKC, MAPKs, and Akt after convulxin stimulation. Honokiol have no cytotoxicity in zebrafish embryos. Honokiol diminished the binding of anti-GP VI (FITC-JAQ1) mAb to human platelets, and it also reduced the coimmunoprecipitation of GP VI-bound Lyn after convulxin stimulation. The surface plasmon resonance results revealed that honokiol binds directly to GP VI, with a K of 289 μM. Platelet function analysis revealed that honokiol substantially prolonged the closure time in human whole blood and increased the occlusion time of thrombotic platelet plug formation in mice. In conclusion, honokiol acts as a potent antagonist of collagen GP VI in human platelets, and it has therapeutic potential in the prevention of the pathological thrombosis.

摘要

厚朴酚来源于木兰科植物，具有多种药理作用。血小板激活在心血管疾病中起着关键作用。已有报道称厚朴酚可抑制胶原刺激的兔血小板聚集。然而，关于厚朴酚在血小板激活中的特征和功能活性的详细进一步研究相对较少。在本研究中，厚朴酚特异性抑制胶原或 convulxin（GP VI 激动剂）刺激引起的血小板聚集和 Ca 离子动员，但不抑制 aggretin（整合素 αβ 激动剂）。厚朴酚还可减轻 convulxin 刺激后 Lyn、PLCγ2、PKC、MAPKs 和 Akt 的磷酸化。厚朴酚在斑马鱼胚胎中无细胞毒性。厚朴酚减少了抗-GP VI（FITC-JAQ1）mAb 与人血小板的结合，并且还减少了 convulxin 刺激后 GP VI 结合的 Lyn 的共免疫沉淀。表面等离子体共振结果表明，厚朴酚直接与 GP VI 结合，Kd 为 289μM。血小板功能分析表明，厚朴酚可显著延长人全血的闭合时间，并增加小鼠血栓性血小板栓子形成的闭塞时间。总之，厚朴酚作为人类血小板中胶原 GP VI 的有效拮抗剂，在预防病理性血栓形成方面具有治疗潜力。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2980/5213647/29f5199c55b4/srep40002-f7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2980/5213647/1c60f4fc2df4/srep40002-f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2980/5213647/d9cfeba91e1f/srep40002-f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2980/5213647/84bfa08caa51/srep40002-f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2980/5213647/0b08e365d240/srep40002-f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2980/5213647/ca84d8353741/srep40002-f5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2980/5213647/138f2c49a809/srep40002-f6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2980/5213647/29f5199c55b4/srep40002-f7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2980/5213647/1c60f4fc2df4/srep40002-f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2980/5213647/d9cfeba91e1f/srep40002-f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2980/5213647/84bfa08caa51/srep40002-f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2980/5213647/0b08e365d240/srep40002-f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2980/5213647/ca84d8353741/srep40002-f5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2980/5213647/138f2c49a809/srep40002-f6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2980/5213647/29f5199c55b4/srep40002-f7.jpg

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