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    Title: Antrodia salmonea inhibits TNF-a-induced angiogenesis and atherogenesis in human endothelial cells through the down-regulation of NF-kB and up-regulation of Nrf2 signaling pathways.
    Authors: 張竣維;Hebron, C.Chang
    Contributors: 生物科技學系
    Date: 2014-01
    Issue Date: 2014-06-04 10:19:17 (UTC+8)
    Abstract: Ethnopharmacological relevance
    Antrodia salmonea (AS) is known as a traditional Chinese medicine, but very few biological activities have been reported.

    Materials and methods
    The present study was aimed to investigate the anti-angiogenic and anti-atherosclerotic potential of the fermented culture broth of AS against tumor necrosis factor-α (TNF-α)-stimulated human endothelial (EA.hy 926) cells.

    The non-cytotoxic concentrations of AS significantly inhibited TNF-α-induced migration/invasion and capillary-like tube formation in EA.hy 926 cells. Furthermore, AS suppressed TNF-α-induced activity and expression of matrix metalloproteinase-9 (MMP-9), and cell-surface expression of intercellular adhesion molecule-1 (ICAM-1), which was associated with abridged adhesion of U937 leukocytes to endothelial cells. Moreover, AS significantly down-regulated TNF-α-induced nuclear translocation and transcriptional activation of nuclear factor κB (NF-κB) followed by suppression of I-κB degradation and phosphorylation of I-κB kinase-α (IKKα). Notably, the protective effect of AS was directly correlated with the increased expression of hemeoxygenase-1 (HO-1) and γ-glutamylcysteine synthetase (γ-GCLC), which was reasoned by nuclear translocation and transactivation of NF-E2 related factor-2 (Nrf2)/antioxidant response element (ARE). Furthermore, HO-1 knockdown by HO-1-specific shRNA diminished the protective effects of AS on TNF-α-stimulated invasion, tube formation, and U937 adhesion in EA.hy 926 cells.

    Taken together, these results suggest that Antrodia salmonea may be useful for the prevention of angiogenesis and atherosclerosis.
    Relation: JOURNAL OF ETHNOPHARMACOLOGY,V.151(1):394–406.
    Appears in Collections:[Department of Biotechnology] Journal Article

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