Amarogentin, a Secoiridoid Glycoside, Abrogates Platelet Activation through PLC gamma 2-PKC and MAPK Pathways

作者：Yen Ting Lin; Lu Wan Jung; Lien Li Ming; Thomas Philip Aloysius; Lee Tzu Yin; Chiu Hou Chang; Sheu Joen Rong^*; Lin Kuan Hung

来源：Biomed Research International, 2014, 2014: 728019.

DOI：10.1155/2014/728019

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 similar to 60 mu M) inhibited platelet aggregation induced by collagen, but not thrombin, arachidonic acid, and U46619. Amarogentin inhibited collagen-induced phosphorylation of phospholipase C (PLC)gamma 2, 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 gamma 2-PKC cascade and MAPK pathway. Our findings suggest that amarogentin may offer therapeutic potential for preventing or treating thromboembolic disorders.

• 出版日期2014
• 单位河北医科大学