• J Ethnopharmacol · Mar 2008

    Blockade of glycoprotein IIb/IIIa mediates the antithrombotic activity of butanol fraction of Actinostemma lobatum Maxim.

    • Kwan-Hyun Kim, Hyo-Jung Lee, Jae-Ho Lee, Yu-Sung Jang, Dae-Keun Kim, Bum-Sang Shim, Ki-Ho Cho, Seong-Gyu Ko, Kyoo-Seok Ahn, and Sung-Hoon Kim.
    • Graduate School of East-West Medical Science, Kyunghee University, Yongin 446-701, Republic of Korea.
    • J Ethnopharmacol. 2008 Mar 28; 116 (3): 431-8.

    Aim Of The StudyActinostemma lobatum Maxim, a wildlife plant of Cucurbitaceae family, has been utilized for the prevention or treatment of cardiovascular diseases as a folk remedy in Korea. However, its scientific evidence remains unclear. Thus, in the present study, we examined the effects of butanol fraction of Actinostemma lobatum Maxim (BFALM) on the in vitro and in vivo antithrombotic activity and possible mechanisms were elucidated for the first time.Material And MethodsTo elucidate the antithrombotic mechanism of BFALM, platelet aggregation assay, coagulation assay, glycoprotein IIb/IIIa assay, thromboxane A(2) assay and in vivo pulmonary thromboembolism experiment were performed.ResultsBFALM significantly inhibited collagen, adenosine diphosphate (ADP) and thrombin-induced platelet aggregation in a concentration dependent manner. Consistently, oral administration of BFALM resulted in a dose-dependent increase of survival rates of mice with pulmonary thromboembolism induced by intravenous injection of collagen and epinephrine. In mechanism assays for the antithrombotic activity of BFALM, BFALM significantly inhibited the fibrinogen binding to the platelet surface Glycoprotein IIb/IIIa (GP IIb/IIIa) receptor in a concentration dependent fashion, as well as reduced the level of thromboxane A(2) at 400microg/ml. Furthermore, BFALM significantly prolonged the prothrombin time (PT) and activated partial thromboplastin time (APTT) compared with untreated control.ConclusionsThese results suggest that BFALM may exert antithrombotic activity through inhibition of platelet aggregation via GP IIb/IIIa and thromboxane A(2) pathways, along with anticoagulatory activity through intrinsic and extrinsic pathways.

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