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

机译:普通小麦。增加胞浆中Ca2 +的浓度并抑制血管内皮细胞中Ca2 +的贮存操作

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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.
机译:这项研究评估了千叶茴香精油的效果。 (茴香油)和茴香脑的主要成分透茴香脑,在细胞外Ca2 +诱导的储库操纵的Ca2 +进入(SOCE)进入血管内皮(EA)细胞及其作用机理。通过气相色谱-质谱法分析茴香油的成分。使用Fura-2荧光测定EA细胞中的胞质Ca2 +浓度([Ca2 +](c))。在细胞外Ca2 +存在下,茴香油显着增加了EA细胞中的[Ca2 +](c)。这种增加被Ca2 +通道阻滞剂La3 +和硝苯地平显着抑制。相反,在不含Ca2 +的溶液中,茴香油诱导的[Ca2 +](c)明显较低,这表明茴香油主要通过增强Ca2 +流入EA细胞的量来增加[Ca2 +](c)。反式茴香脑[Ca2 +](c)动员与茴香油相似。此外,茴香油和反茴香被抑制了SOCE。 SOCE也被非选择性阳离子通道(NSC)阻断剂镧(La3 +)衰减。 2-氨基乙氧基二苯基硼烷(2-APB),一种肌醇1,4,5-三磷酸(IP3)受体抑制剂和SOCE阻滞剂; U73122,磷脂酶C(PLC)的抑制剂。此外,与单独使用La3 +相比,La3 +加茴香油或反式茴香脑对SOCE的抑制作用更强。这些发现表明茴香油和茴香脑可显着抑制SOCE诱导的血管内皮细胞中[Ca2 +] c的增加,并且这些反应可能是由NSC,依赖IP3的Ca2 +动员和PLC激活介导的。 (C)2016 Elsevier Masson SAS。版权所有。

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