Effects of curcumin, a biologically active ingredient of turmeric, were tested on the Ca²⁺ transients induced by the activation of α₇ subunit of the human nicotinic acetylcholine (α₇ nACh) receptor expressed in SH-EP1 cells. Curcumin caused a significant potentiation of choline (1 mM)-induced Ca²⁺ transients with an EC₅₀ value of 133 nM. The potentiating effect of curcumin was not observed in Ca²⁺ transients induced by high K⁺ (60 mM) containing solutions or activation of α₄β₂ nACh receptors and the extent of curcumin potentiation was not altered in the presence of Ca²⁺ 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 Ca²⁺ 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 Ca²⁺ transients. Notably, specific binding of [¹²⁵I]-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.

姜黄素，姜黄生物活性成分的影响，进行了对测试的Ca ²⁺由α的激活诱导的瞬变₇亚基人烟碱乙酰胆碱（α ₇胆碱）在SH-EP1细胞中表达的受体。姜黄素引起胆碱（1 mM）诱导的Ca ²⁺瞬变的显着增强，EC ₅₀值为133 nM。在钙没有观察到姜黄素的增强作用²⁺由高K值引起的瞬变⁺含有溶液或α活化（60毫摩尔）₄ β ₂ nACh受体和姜黄素增强的程度在Ca的存在没有改变²⁺通道拮抗剂硝苯地平（1μM），维拉帕米（1μM），ω-芋螺毒素（1μM）和苯普地尔（10μM）。值得注意的是，在未进行姜黄素预温育的情况下，同时使用姜黄素和胆碱时，未观察到姜黄素的作用。姜黄素对胆碱诱导的Ca ²⁺瞬变的作用没有通过与蛋白C，A和CaM激酶抑制剂的预孵育而逆转。姜黄素的代谢产物，如四氢姜黄素，去甲基姜黄素和二去甲基姜黄素也可增强胆碱诱导的Ca ²⁺瞬变。值得注意的是，在姜黄素的存在下[ ¹²⁵ I]-真菌毒素的特异性结合没有改变。总体而言，我们的结果表明姜黄素能变构地增强SH-EP1细胞中表达的α7-nACh受体的功能。