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Foeniculum vulgare Mill. increases cytosolic Ca2+ concentration and inhibits store-operated Ca2+ entry in vascular endothelial cells

Authors
Han, A. YoungLee, Hui SuSeol, Geun Hee
Issue Date
12월-2016
Publisher
ELSEVIER FRANCE-EDITIONS SCIENTIFIQUES MEDICALES ELSEVIER
Keywords
Foeniculum vulgare Mill.; trans-anethole; Store-operated Ca2+ entry; Cytosolic Ca2+; Vascular endothelial cells
Citation
BIOMEDICINE & PHARMACOTHERAPY, v.84, pp.800 - 805
Indexed
SCIE
SCOPUS
Journal Title
BIOMEDICINE & PHARMACOTHERAPY
Volume
84
Start Page
800
End Page
805
URI
https://scholar.korea.ac.kr/handle/2021.sw.korea/86685
DOI
10.1016/j.biopha.2016.10.013
ISSN
0753-3322
Abstract
This study assessed the effects of essential oil of Foeniculum vulgare Mill. (fennel oil) and of transanethole, the main component of fennel oil, on extracellular Ca2+-induced store-operated Ca2+ entry (SOCE) into vascular endothelial (EA) cells and their mechanisms of action. Components of fennel oil were analyzed by gas chromatography-mass spectrometry. Cytosolic Ca2+ concentration ([Ca2+](c)) in EA cells was determined using Fura-2 fluorescence. In the presence of extracellular Ca2+, fennel oil significantly increased [Ca2+](c) in EA cells; this increase was significantly inhibited by the Ca2+ channel blockers La3+ and nifedipine. In contrast, fennel oil induced [Ca2+](c) was significantly lower in Ca2+-free solution, suggesting that fennel oil increases [Ca2+](c) mainly by enhancing Ca2+ influx into EA cells. [Ca2+](c) mobilization by trans-anethole was similar to that of fennel oil. Moreover, SOCE was suppressed by fennel oil and trans-anethole. SOCE was also attenuated by lanthanum (La3+), a non-selective cation channel (NSC) blocker; 2-aminoethoxydiphenyl borane (2-APB), an inositol 1,4,5-triphosphate (IP3) receptor inhibitor and SOCE blocker; and U73122, an inhibitor of phospholipase C (PLC). Further, SOCE was more strongly inhibited by La3+ plus fennel oil or trans-anethole than by La3+ alone. These findings suggest that fennel oil and trans-anethole significantly inhibit SOCE-induced [Ca2+] c increase in vascular endothelial cells and that these reactions may be mediated by NSC, IP3-dependent Ca2+ mobilization, and PLC activation. (C) 2016 Elsevier Masson SAS. All rights reserved.
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Seol, Geun Hee
간호대학 (간호학과)
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