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苦味叶下珠素，一种裂环烯醚萜苷，通过PLCγ2-PKC和MAPK途径消除血小板活化。

Amarogentin, a secoiridoid glycoside, abrogates platelet activation through PLC γ 2-PKC and MAPK pathways.

作者信息

Yen Ting-Lin, Lu Wan-Jung, Lien Li-Ming, Thomas Philip Aloysius, Lee Tzu-Yin, Chiu Hou-Chang, Sheu Joen-Rong, Lin Kuan-Hung

机构信息

Graduate Institute of Medical Sciences and Department of Pharmacology, College of Medicine, Taipei Medical University, 250 Wu-Hsing Street, Taipei 110, Taiwan.

School of Medicine, Taipei Medical University, 250 Wu-Hsing Street, Taipei 110, Taiwan ; Department of Neurology, Shin Kong Wu Ho-Su Memorial Hospital, 95 Wen-Chang Road, Taipei 111, Taiwan.

出版信息

Biomed Res Int. 2014;2014:728019. doi: 10.1155/2014/728019. Epub 2014 Apr 29.

DOI:10.1155/2014/728019
PMID:24868545
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4020542/
Abstract

Amarogentin, an active principle of Gentiana lutea, possess antitumorigenic, antidiabetic, and antioxidative properties. Activation of platelets is associated with intravascular thrombosis and cardiovascular diseases. The present study examined the effects of amarogentin on platelet activation. Amarogentin treatment (15~60  μM) inhibited platelet aggregation induced by collagen, but not thrombin, arachidonic acid, and U46619. Amarogentin inhibited collagen-induced phosphorylation of phospholipase C (PLC) γ2, protein kinase C (PKC), and mitogen-activated protein kinases (MAPKs). It also inhibits in vivo thrombus formation in mice. In addition, neither the guanylate cyclase inhibitor ODQ nor the adenylate cyclase inhibitor SQ22536 affected the amarogentin-mediated inhibition of platelet aggregation, which suggests that amarogentin does not regulate the levels of cyclic AMP and cyclic GMP. In conclusion, amarogentin prevents platelet activation through the inhibition of PLC γ2-PKC cascade and MAPK pathway. Our findings suggest that amarogentin may offer therapeutic potential for preventing or treating thromboembolic disorders.

摘要

苦味龙胆酯苷是龙胆的一种活性成分，具有抗肿瘤、抗糖尿病和抗氧化特性。血小板的激活与血管内血栓形成和心血管疾病有关。本研究考察了苦味龙胆酯苷对血小板激活的影响。苦味龙胆酯苷处理（15~60 μM）可抑制胶原蛋白诱导的血小板聚集，但对凝血酶、花生四烯酸和U46619诱导的血小板聚集无抑制作用。苦味龙胆酯苷可抑制胶原蛋白诱导的磷脂酶C（PLC）γ2、蛋白激酶C（PKC）和丝裂原活化蛋白激酶（MAPK）的磷酸化。它还可抑制小鼠体内血栓形成。此外，鸟苷酸环化酶抑制剂ODQ和腺苷酸环化酶抑制剂SQ22536均不影响苦味龙胆酯苷介导的血小板聚集抑制作用，这表明苦味龙胆酯苷不调节环磷酸腺苷（cAMP）和环磷酸鸟苷（cGMP）水平。总之，苦味龙胆酯苷通过抑制PLC γ2-PKC级联反应和MAPK途径来防止血小板激活。我们的研究结果表明，苦味龙胆酯苷可能为预防或治疗血栓栓塞性疾病提供治疗潜力。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/de0e/4020542/db4a4b99a714/BMRI2014-728019.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/de0e/4020542/c7e69e059fa7/BMRI2014-728019.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/de0e/4020542/76fdcca4d737/BMRI2014-728019.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/de0e/4020542/dc60b22d5132/BMRI2014-728019.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/de0e/4020542/174b518702bf/BMRI2014-728019.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/de0e/4020542/db4a4b99a714/BMRI2014-728019.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/de0e/4020542/c7e69e059fa7/BMRI2014-728019.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/de0e/4020542/76fdcca4d737/BMRI2014-728019.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/de0e/4020542/dc60b22d5132/BMRI2014-728019.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/de0e/4020542/174b518702bf/BMRI2014-728019.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/de0e/4020542/db4a4b99a714/BMRI2014-728019.005.jpg

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