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Year : 2019  |  Volume : 5  |  Issue : 4  |  Page : 260-268

Effects of water-soluble tomato concentrate on platelet aggregation

1 Center for Biomechanopharmacology, Institute of Chinese Materia Medica, China Academy of Chinese Medical Sciences, Beijing, China
2 Science and Technology Center, ByHealth Co., Ltd., Guangzhou, China
3 Department of Cardiovascular, Dongzhimen Hospital, Beijing University of Chinese Medicine, Beijing, China

Correspondence Address:
Prof. Yun You
Institute of Chinese Materia Medica, China Academy of Chinese Medical Sciences, Beijing 100700
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/wjtcm.wjtcm_35_19

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Objective: To investigate the antiplatelet aggregation effect of water-soluble tomato concentrate (WSTC) and explore the underlying molecular mechanisms. Materials and Methods: Platelet aggregometry was used to quantify rat platelet aggregation with the maximum aggregation rate in vitro and ex vivo. Then, the fibrinogen (FIB) binding assay was employed to detect the effect of WSTC on the activation of platelet integrin αIIβ3 (GP IIb/IIIa). Furthermore, Western blot was performed to assess the platelet protein levels of phosphoinositide 3-kinase 110 β (PI3K110 β), protein disulfide isomerase (PDI), platelet endothelial cell adhesion molecule 1 (PECAM-1), and β1-Tubulin. Results: WSTC inhibited adenosine diphosphate (ADP) and collagen-induced platelet aggregation in a concentration-dependent manner in vitro, at IC50values of 3.05 g/L and 8.03 g/L, respectively. Significantly reduced ex vivo ADP induced platelet aggregation was observed after oral consumption of WSTC for 4 weeks in rats; average inhibition rates were 24.42%, 21.48%, and 20.87% for 25 mg/Kg, 75 mg/Kg, and 150 mg/Kg WSTC, respectively. It appeared that WSTC had no influence on coagulation function in rats. Incubation with WSTC decreased FIB binding to GP IIb/IIIa by 17.47% and 32.29% at the concentrations of 0.6 and 6 g/L, respectively. WSTC at 0.6 and 6 g/L markedly downregulated PI3K110 β, PDI, and PECAM-1 in platelets, and upregulated β1-Tubulin, in a concentration-dependent manner. Conclusion: WSTC inhibits platelet activation through modulation of platelet skeletal stability and suppresses GP IIb/IIIa receptor-mediated platelet aggregation, likely via the PI3K signaling pathway and PDI inhibition.

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