Effects of (1R,9S)-[beta]-Hydrastine on Intracellular Calcium Concentration in PC12 Cells

(1R,9S)-β-Hydrastine (BHS) decreases the basal intracellular Ca2+ concentration ([Ca2+]i) in PC12 cells.5) This study examined the effects of (1R,9S)-BHS on [Ca2+]i in PC12 cells. (1R,9S)-BHS at 10--100 μM in combination with a high extracellular K+ level (56 mM) inhibited the release of dopamine in...

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Published inBiological & pharmaceutical bulletin Vol. 30; no. 8; p. 1547
Main Authors Yu Yin, Shou, Mi Kim, Yu, Joon Lee, Jae, Mei Jin, Chun, Jung Yang, Yoo, Park, Seung-Kook, Kuel Yoo, Se, Koo Lee, Myung
Format Journal Article
LanguageEnglish
Published Tokyo Japan Science and Technology Agency 01.08.2007
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Abstract (1R,9S)-β-Hydrastine (BHS) decreases the basal intracellular Ca2+ concentration ([Ca2+]i) in PC12 cells.5) This study examined the effects of (1R,9S)-BHS on [Ca2+]i in PC12 cells. (1R,9S)-BHS at 10--100 μM in combination with a high extracellular K+ level (56 mM) inhibited the release of dopamine in a concentration-dependent manner with an IC50 value of 66.5 μM. BHS at 100 μM inhibited the sustained increase in [Ca2+]i induced by a high K+ level (56 mM), and had an inhibitory effect on the 2 μM nifedipine-induced blockage of the K+-stimulated sustained increase in [Ca2+]i. In addition, (1R,9S)-BHS at 100 μM prevented the rapid and sustained increase in [Ca2+]i elicited by 20 mM caffeine, but did not have an effect on the increase induced by 1 μM thapsigargin, in the presence of external Ca2+. These results suggest that the active sites of (1R,9S)-BHS are mainly L-type Ca2+ channels and caffeine-sensitive Ca2+-permeable channels in PC12 cells.
AbstractList (1R,9S)-β-Hydrastine (BHS) decreases the basal intracellular Ca2+ concentration ([Ca2+]i) in PC12 cells.5) This study examined the effects of (1R,9S)-BHS on [Ca2+]i in PC12 cells. (1R,9S)-BHS at 10--100 μM in combination with a high extracellular K+ level (56 mM) inhibited the release of dopamine in a concentration-dependent manner with an IC50 value of 66.5 μM. BHS at 100 μM inhibited the sustained increase in [Ca2+]i induced by a high K+ level (56 mM), and had an inhibitory effect on the 2 μM nifedipine-induced blockage of the K+-stimulated sustained increase in [Ca2+]i. In addition, (1R,9S)-BHS at 100 μM prevented the rapid and sustained increase in [Ca2+]i elicited by 20 mM caffeine, but did not have an effect on the increase induced by 1 μM thapsigargin, in the presence of external Ca2+. These results suggest that the active sites of (1R,9S)-BHS are mainly L-type Ca2+ channels and caffeine-sensitive Ca2+-permeable channels in PC12 cells.
Author Yu Yin, Shou
Mei Jin, Chun
Kuel Yoo, Se
Jung Yang, Yoo
Mi Kim, Yu
Park, Seung-Kook
Koo Lee, Myung
Joon Lee, Jae
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