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논문 기본 정보

자료유형
학술저널
저자정보
Yin, Shou Yu (College of Pharmacy, Yanbian University) Jin, Chun-Mei (College of Pharmacy, and Research Center for Bioresource and Health, Chungbuk National University) Yang, Yoo-Jung (College of Pharmacy, and Research Center for Bioresource and Health, Chungbuk National University) Lim, Sung-Cil (College of Pharmacy, and Research Center for Bioresource and Health, Chungbuk National University) Lee, Chong-Kil (College of Pharmacy, and Research Center for Bioresource and Health, Chungbuk National University) Hwang, Bang-Yeon (College of Pharmacy, and Research Center for Bioresource and Health, Chungbuk National University) Ro, Jai-Seup (College of Pharmacy, and Research Center for Bioresource and Health, Chungbuk National University) Lee, Myung-Koo (College of Pharmacy, and Research Center for Bioresource and Health, Chungbuk National University)
저널정보
대한약학회 Archives of pharmacal research : a publication of the Pharmaceutical Society of Korea Archives of pharmacal research : a publication of the Pharmaceutical Society of Korea 제30권 제1호
발행연도
2007.1
수록면
109 - 113 (5page)

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[ $(1R,9S)-{\beta} ]-Hydrastine$ (BHS), at $100{\mu}M$, has been shown to mainly reduce the $K^+-induced$ dopamine release and $Ca^{2+}$ influx by blocking the L-type $Ca^{2+}$ channel and inhibit the caffeine activated store-operated $Ca^{2+}$ channels, but not those activated by thapsigargin, in PC12 cells. In this study, the effects of BHS on $Ca^{2+}$ transport from $Ca^{2+}$ stores in the absence of external $Ca^{2+}$ were investigated in PC12 cells. BHS decreased the basal intracellular $Ca^{2+}$ concentration $([Ca^{2+}]_i)$ in the absence of external $Ca^{2+}$ in PC12 cells. In the absence of external $Ca^{2+}$, pre-treating PC12 cells with $100{\mu}M$ BHS reduced the rapid increase in the $[Ca^{2+}]_i$ elicited by 20mM caffeine, but not that by $1{\mu}M$ thapsigargin. In addition, BHS inhibited the increase in the $[Ca^{2+}]_i$ elicited by restoration of 2mM $CaCl_2$ after the $Ca^{2+}$ stores had been depleted by 20mM caffeine, but not those depleted by $1{\mu}M$ thapsigargin, in the absence of external $Ca^{2+}$. These results suggested that BHS mainly inhibited $Ca^{2+}$ leakage from the $Ca^{2+}$ stores and the caffeine-stimulated release of $Ca^{2+}$ from the caffeine-sensitive $Ca^{2+}$ stores in PC12 cells.

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