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

A. Young Han, Hui Su Lee, Geun Hee Seol

Research output: Contribution to journalArticle

2 Citations (Scopus)

Abstract

This study assessed the effects of essential oil of Foeniculum vulgare Mill. (fennel oil) and of trans-anethole, 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.

Original languageEnglish
Pages (from-to)800-805
Number of pages6
JournalBiomedicine and Pharmacotherapy
Volume84
DOIs
Publication statusPublished - 2016 Dec 1

Fingerprint

Foeniculum
Endothelial Cells
Oils
Type C Phospholipases
Cations
Boranes
Inositol 1,4,5-Trisphosphate Receptors
Lanthanum
Inositol 1,4,5-Trisphosphate
Fura-2
Volatile Oils
Nifedipine
Gas Chromatography-Mass Spectrometry

Keywords

  • Cytosolic Ca
  • Foeniculum vulgare Mill.
  • Store-operated Ca entry
  • trans-anethole
  • Vascular endothelial cells

ASJC Scopus subject areas

  • Pharmacology

Cite this

Foeniculum vulgare Mill. increases cytosolic Ca2+ concentration and inhibits store-operated Ca2+ entry in vascular endothelial cells. / Han, A. Young; Lee, Hui Su; Seol, Geun Hee.

In: Biomedicine and Pharmacotherapy, Vol. 84, 01.12.2016, p. 800-805.

Research output: Contribution to journalArticle

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abstract = "This study assessed the effects of essential oil of Foeniculum vulgare Mill. (fennel oil) and of trans-anethole, 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.",
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N2 - This study assessed the effects of essential oil of Foeniculum vulgare Mill. (fennel oil) and of trans-anethole, 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.

AB - This study assessed the effects of essential oil of Foeniculum vulgare Mill. (fennel oil) and of trans-anethole, 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.

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