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Please use this identifier to cite or link to this item:
http://140.112.115.32:8080/ir/handle/987654321/2765
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| Title: | Amarogentin, a Secoiridoid Glycoside, Abrogates Platelet Activation through PLCγ2-PKC and MAPK Pathways |
| Authors: | Ting-Lin Yen;Wan-Jung Lu;Li-Ming Lien;Philip Aloysius Thomas;Tzu-Yin Lee;Hou-Chang Chiu;Joen-Rong Sheu;Kuan-Hung Lin |
| Contributors: | 視光學系 |
| Date: | 2014-04-01 |
| Issue Date: | 2025-08-01 15:06:56 (UTC+8) |
| 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 PLCγ2-PKC cascade and MAPK pathway. Our findings suggest that amarogentin may offer therapeutic potential for preventing or treating thromboembolic disorders. |
| Relation: | BioMed Research International, 2014(1), 728019. https://doi.org/10.1155/2014/728019 |
| Appears in Collections: | [視光學系] 期刊論文
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