ORCID Identifiers

0000-0002-3231-6291

Document Type

Article

Source of Publication

Neurochemistry International

Publication Date

3-1-2018

Abstract

© 2018 Elsevier Ltd Effects of curcumin, a biologically active ingredient of turmeric, were tested on the Ca 2+ transients induced by the activation of α 7 subunit of the human nicotinic acetylcholine (α 7 nACh) receptor expressed in SH-EP1 cells. Curcumin caused a significant potentiation of choline (1 mM)-induced Ca 2+ transients with an EC 50 value of 133 nM. The potentiating effect of curcumin was not observed in Ca 2+ transients induced by high K + (60 mM) containing solutions or activation of α 4 β 2 nACh receptors and the extent of curcumin potentiation was not altered in the presence of Ca 2+ channel antagonists nifedipine (1 μM), verapamil (1 μM), ω-conotoxin (1 μM), and bepridil (10 μM). Noticeably the effect of curcumin was not observed when curcumin and choline were co-applied without curcumin pre-incubation. The effect of curcumin on choline-induced Ca 2+ transients was not reversed by pre-incubation with inhibitors of protein C, A, and CaM kinases. Metabolites of curcumin such as tetrahydrocurcumin, demethylcurcumin, and didemethylcurcumin also caused potentiation of choline-induced Ca 2+ transients. Notably, specific binding of [ 125 I]-bungarotoxin was not altered in the presence of curcumin. Collectively, our results indicate that curcumin allosterically potentiate the function of the α7-nACh receptor expressed in SH-EP1 cells.

ISSN

0197-0186

Publisher

Elsevier Ltd

Volume

114

First Page

80

Last Page

84

Disciplines

Life Sciences | Medicine and Health Sciences

Keywords

Choline, Curcumin, Intracellular calcium, Nicotinic receptors

Scopus ID

85041507122

Indexed in Scopus

yes

Open Access

yes

Open Access Type

Green: A manuscript of this publication is openly available in a repository

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