Takemura H, Kwan C Y, Ohshika H
Department of Pharmacology, School of Medicine, Sapporo Medical University, Japan.
Res Commun Mol Pathol Pharmacol. 1995 Oct;90(1):59-68.
We examined the effects of tetrandrine (TET) on Ca2+ mobilization in various types of cells using inositol trisphosphate-generating drugs and compared it with those using the microsomal Ca(2+)-ATPase inhibitor thapsigargin (TG) which is a tool for analyzing Ca2+ store-regulated Ca2+ entry (capacitative Ca2+ entry). In rat pheochromocytoma PC12 cells, 100 microM TET abolished high K+ (30 mM)-induced sustained increase in [Ca2+]i and partially inhibited bradykinin (1 microM)-induced or TG (100 nM)-induced Ca2+ entry. In NIH/3T3 fibroblasts, 100 microM TET abolished Ca2+ entry induced by bombesin (1 microM) or TG (100 nM). In rat glioma C6 cells, the addition of 100 microM TET reduced the sustained elevation of [Ca2+]i induced by endothelin 1 (10 nM) or TG (100 nM) declining to the resting level. In rat parotid acinar cells, 100 microM TET abolished a sustained increase in [Ca2+]i induced by carbachol (100 microM) or TG (100 nM). In human leukemia T-cell line Jurkat, 100 microM TET did not inhibit Ca2+ entry evoked by the anti-CD3 antibody OKT3 (10 micrograms/ml) or TG (100 nM). The present results suggest that the action of TET on Ca2+ entry is dependent on cell types.
我们使用生成肌醇三磷酸的药物研究了粉防己碱（TET）对各类细胞中Ca2+动员的影响，并将其与使用微粒体Ca(2+)-ATP酶抑制剂毒胡萝卜素（TG）的情况进行比较，TG是一种用于分析Ca2+储存调节的Ca2+内流（容量性Ca2+内流）的工具。在大鼠嗜铬细胞瘤PC12细胞中，100μM TET消除了高钾（30 mM）诱导的[Ca2+]i持续升高，并部分抑制了缓激肽（1μM）诱导的或TG（100 nM）诱导的Ca2+内流。在NIH/3T3成纤维细胞中，100μM TET消除了蛙皮素（1μM）或TG（100 nM）诱导的Ca2+内流。在大鼠胶质瘤C6细胞中，添加100μM TET可降低内皮素1（10 nM）或TG（100 nM）诱导的[Ca2+]i持续升高，并降至静息水平。在大鼠腮腺腺泡细胞中，100μM TET消除了卡巴胆碱（100μM）或TG（100 nM）诱导的[Ca2+]i持续升高。在人白血病T细胞系Jurkat中，100μM TET不抑制抗CD3抗体OKT3（10μg/ml）或TG（100 nM）诱发的Ca2+内流。目前的结果表明，TET对Ca2+内流的作用取决于细胞类型。
