[This retracts the article DOI: 10.3892/ol.2016.5474.].
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http://dx.doi.org/10.3892/ol.2023.14173 | DOI Listing |
Biomed Pharmacother
October 2020
Department of Pharmacology and Intractable Disease Research Center, School of Medicine, Dongguk University, Gyeongju, Gyeongsangbuk-do 38066, Republic of Korea. Electronic address:
Pathophysiological reaction of platelets in the blood vessel is an indispensable part of thrombosis and cardiovascular disease, which is the most common cause of death in the world. In this study, we performed in vitro assays to evaluate antiplatelet activity of arctigenin in human platelets and attempted to identify the mechanism responsible for thromboxane A (TXA) generation, integrin αβ activation and cAMP pathway. Arctigenin exhibited obvious inhibitory effects on collagen-, thrombin-, and ADP-induced human platelet aggregation, granule secretion, TXA generation, integrin αβ activation, and clot retraction.
View Article and Find Full Text PDFOncol Lett
February 2017
Department of Neurosurgery, The First Affiliated Hospital of Xinjiang Medical University, Ürümqi, Xinjiang Uyghur Autonomous Region 830054, P.R. China.
The aim of the current study was to investigate the anticancer potential of arctigenin, a natural lignan compound, in malignant gliomas. The U87MG and T98G human glioma cell lines were treated with various concentrations of arctigenin for 48 h and the effects of arctigenin on the aggressive phenotypes of glioma cells were assessed. The results demonstrated that arctigenin dose-dependently inhibited the growth of U87MG and T98G cells, as determined using 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide and bromodeoxyuridine incorporation assays.
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