Curcumin potentiates the function of human α ₇ -nicotinic acetylcholine receptors expressed in SH-EP1 cells

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.