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香柠檬(Citrus bergamia Risso)通过从主要细胞内库释放 Ca(2+)来升高人血管内皮细胞内的 Ca(2+)。

Citrus bergamia Risso Elevates Intracellular Ca (2+) in Human Vascular Endothelial Cells due to Release of Ca (2+) from Primary Intracellular Stores.

机构信息

Department of Basic Nursing Science, School of Nursing, Korea University, 145 Anam-ro, Seongbuk-gu, Seoul 136-701, Republic of Korea.

Department of Physiology and Biophysics, School of Medicine, Eulji University, Youngdu-dong, Jung-gu, Daejeon 301-746, Republic of Korea.

出版信息

Evid Based Complement Alternat Med. 2013;2013:759615. doi: 10.1155/2013/759615. Epub 2013 Nov 21.

Abstract

The purpose of the present study is to examine the effects of essential oil of Citrus bergamia Risso (bergamot, BEO) on intracellular Ca(2+) in human umbilical vein endothelial cells. Fura-2 fluorescence was used to examine changes in intracellular Ca(2+) concentration [Ca(2+)]i . In the presence of extracellular Ca(2+), BEO increased [Ca(2+)]i , which was partially inhibited by a nonselective Ca(2+) channel blocker La(3+). In Ca(2+)-free extracellular solutions, BEO increased [Ca(2+)]i in a concentration-dependent manner, suggesting that BEO mobilizes intracellular Ca(2+). BEO-induced [Ca(2+)]i increase was partially inhibited by a Ca(2+)-induced Ca(2+) release inhibitor dantrolene, a phospholipase C inhibitor U73122, and an inositol 1,4,5-triphosphate (IP3)-gated Ca(2+) channel blocker, 2-aminoethoxydiphenyl borane (2-APB). BEO also increased [Ca(2+)]i in the presence of carbonyl cyanide m-chlorophenylhydrazone, an inhibitor of mitochondrial Ca(2+) uptake. In addition, store-operated Ca(2+) entry (SOC) was potentiated by BEO. These results suggest that BEO mobilizes Ca(2+) from primary intracellular stores via Ca(2+)-induced and IP3-mediated Ca(2+) release and affect promotion of Ca(2+) influx, likely via an SOC mechanism.

摘要

本研究旨在探讨香柠檬(bergamot,BEO)精油对人脐静脉内皮细胞内钙离子(Ca(2+))浓度的影响。利用 Fura-2 荧光探针检测细胞内 Ca(2+)浓度 ([Ca(2+)]i) 的变化。在存在细胞外 Ca(2+)的情况下,BEO 增加了 [Ca(2+)]i,这一过程被非选择性钙通道阻滞剂 La(3+)部分抑制。在无细胞外 Ca(2+)的溶液中,BEO 浓度依赖性地增加了 [Ca(2+)]i,提示 BEO 动员了细胞内 Ca(2+)。BEO 诱导的 [Ca(2+)]i 增加被钙诱导钙释放抑制剂 dantrolene、PLC 抑制剂 U73122 和 IP3 门控 Ca(2+)通道阻滞剂 2-APB 部分抑制。BEO 还增加了线粒体 Ca(2+)摄取抑制剂羰基氰化物 m-氯苯腙存在下的 [Ca(2+)]i。此外,BEO 增强了 SOC 介导的 Ca(2+)内流。这些结果表明,BEO 通过 Ca(2+)诱导和 IP3 介导的 Ca(2+)释放从细胞内主要储存库动员 Ca(2+),并影响 Ca(2+)内流的促进,可能通过 SOC 机制。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e98f/3857908/7642f2c8e15c/ECAM2013-759615.001.jpg

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