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NEUROPHARMACOLOGY

Phytoestrogen Cimicifugoside-Mediated Inhibition of Catecholamine Secretion by Blocking Nicotinic Acetylcholine Receptor in Bovine Adrenal Chromaffin Cells

Department of Life Science (K.C.W., Y.S.P., D.J.J., K.T.K.), Division of Molecular and Life Science, Pohang University of Science and Technology, Pohang, South Korea; Department of Life Science and Food Engineering (K.C.W., B.S.S.), Handong Global University, Pohang, South Korea; Medical Research Institute (J.O.L.), School of Medicine, Kyungpook National University, Daegu, South Korea; Department of Anesthesiology (W.Y.B.), School of Medicine, Kyungpook National University, Daegu, South Korea

We investigated the effect of the phytoestrogen cimicifugoside, one of the pharmacologically active ingredients of the medicinal plant Cimicifuga racemosa (black cohosh) that has been used to treat many kinds of neuronal and menopausal symptoms, such as arthritis, menopausal depression, and nerve pain. Cimicifugoside inhibited calcium increase induced by 1,1-dimethyl-4-phenylpiperazinium iodide (DMPP), a nicotinic acetylcholine receptor (nAChR) agonist in bovine adrenal chromaffin cells with a half-maximal inhibitory concentration (IC₅₀) of 18 ± 2 µM. In contrast, cimicifugoside did not affect the calcium increases evoked by high K⁺, veratridine, and bradykinin. The DMPP-induced sodium increase was also inhibited by cimicifugoside with an IC₅₀ of 2 ± 0.3 µM, suggesting that the activity of nAChRs is inhibited by cimicifugoside. Cimicifugoside did not affect the KCl-induced secretion but markedly inhibited the DMPP-induced catecholamine secretion that was monitored by carbon-fiber amperometry in real time and high-performance liquid chromatography through electrochemical detection. The results suggest that cimicifugoside selectively inhibits nAChR-mediated response in bovine chromaffin cells.

Address correspondence to: Dr. Kyong-Tai Kim, Department of Life Science, POSTECH, San 31, Hyoja Dong, Pohang, 790-784, Korea. E-mail: ktk{at}postech.ac.kr