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Evidence-Based Complementary and Alternative Medicine
Volume 2013 (2013), Article ID 759615, 7 pages
Research Article

Citrus bergamia Risso Elevates Intracellular Ca2+ in Human Vascular Endothelial Cells due to Release of Ca2+ from Primary Intracellular Stores

1Department of Basic Nursing Science, School of Nursing, Korea University, 145 Anam-ro, Seongbuk-gu, Seoul 136-701, Republic of Korea
2Department of Physiology and Biophysics, School of Medicine, Eulji University, Youngdu-dong, Jung-gu, Daejeon 301-746, Republic of Korea
3KT&G Research Institute, Daejeon 305-805, Republic of Korea

Received 26 June 2013; Revised 28 October 2013; Accepted 28 October 2013

Academic Editor: Mohamed Eddouks

Copyright © 2013 Purum Kang et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


The purpose of the present study is to examine the effects of essential oil of Citrus bergamia Risso (bergamot, BEO) on intracellular Ca2+ in human umbilical vein endothelial cells. Fura-2 fluorescence was used to examine changes in intracellular Ca2+ concentration . In the presence of extracellular Ca2+, BEO increased , which was partially inhibited by a nonselective Ca2+ channel blocker La3+. In Ca2+-free extracellular solutions, BEO increased in a concentration-dependent manner, suggesting that BEO mobilizes intracellular Ca2+. BEO-induced increase was partially inhibited by a Ca2+-induced Ca2+ release inhibitor dantrolene, a phospholipase C inhibitor U73122, and an inositol 1,4,5-triphosphate (IP3)-gated Ca2+ channel blocker, 2-aminoethoxydiphenyl borane (2-APB). BEO also increased in the presence of carbonyl cyanide m-chlorophenylhydrazone, an inhibitor of mitochondrial Ca2+ uptake. In addition, store-operated Ca2+ entry (SOC) was potentiated by BEO. These results suggest that BEO mobilizes Ca2+ from primary intracellular stores via Ca2+-induced and IP3-mediated Ca2+ release and affect promotion of Ca2+ influx, likely via an SOC mechanism.