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首页> 外文期刊>Life sciences >The anti-anginal drug fendiline elevates cytosolic Ca(2+) in rabbit corneal epithelial cells.
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The anti-anginal drug fendiline elevates cytosolic Ca(2+) in rabbit corneal epithelial cells.

机译：抗心绞痛药物fendiline升高兔角膜上皮细胞中的胞质Ca（2+）。

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摘要

The effect of the anti-anginal drug fendiline on intracellular free Ca(2+) levels ([Ca(2+)](i)) in a rabbit corneal epithelial cell line (SIRC) was explored using fura-2 as a fluorescent Ca(2+) indicator. At a concentration above 1 microM, fendiline increased [Ca(2+)](i) in a concentration-dependent manner with an EC(50) value of 7 microM. The [Ca(2+)](i) response consisted of an immediate rise and an elevated phase. Extracellular Ca(2+) removal decreased half of the [Ca(2+)](i )signal. Fendiline induced quench of fura-2 fluorescence by Mn(2+) (50 microM), suggesting the presence of Ca(2+) influx across the plasma membrane. This Ca(2+) influx was abolished by La(3+) (50 microM), but was insensitive to dihydropyridines, verapamil and diltiazem. Fendiline (10 microM)-induced store Ca(2+) release was largely reduced by pretreatment with thapsigargin (1 microM) (an endoplasmic reticulum Ca(2+) pump inhibitor) to deplete the endoplasmic reticulum Ca(2+). Conversely, pretreatment with 10 microM fendiline abolished thapsigargin-induced Ca(2+) release. Fendiline (10 microM)-induced Ca(2+) release was not altered by inhibiting phospholipase C with 2 microM 1-(6-((17beta-3-methoxyestra-1,3,5(10)-trien-17-yl)amino)hexyl)-1H-pyrrole -2,5-dione (U73122). Cumulatively, this study shows that fendiline induced concentration-dependent [Ca(2+)](i )increases in corneal epithelial cells by releasing the endoplasmic reticulum Ca(2+) in a phospholipase C-independent manner, and by causing Ca(2+) influx.
机译：探索了抗心绞痛药物芬迪林对兔角膜上皮细胞系（SIRC）中细胞内游离Ca（2+）水平（[Ca（2 +）]（i））的影响，使用fura-2作为荧光Ca （2+）指示器。在高于1 microM的浓度下，fendiline以浓度依赖的方式增加[Ca（2 +）]（i），EC（50）值为7 microM。 [Ca（2 +）]（i）响应包括立即上升和上升阶段。细胞外Ca（2+）去除减少了[Ca（2 +）]（i）信号的一半。芬迪林通过Mn（2+）（50 microM）诱导呋喃2荧光的猝灭，表明整个质膜存在Ca（2+）流入。该Ca（2+）涌入被La（3+）（50 microM）取消，但对二氢吡啶，维拉帕米和地尔硫卓不敏感。苯丁胺（10 microM）诱导的存储Ca（2+）释放大大减少了用thapsigargin（1 microM）（内质网Ca（2+）泵抑制剂）预处理以耗尽内质网Ca（2+）。相反，用10 microM芬迪林进行的预处理废除了thapsigargin诱导的Ca（2+）释放。苯丁胺（10 microM）诱导Ca（2+）释放不会通过抑制磷脂酶C与2 microM 1-（6-（（17beta-3-methoxyestra-1,3,5（10）-trien-17-yl ）氨基）己基）-1H-吡咯-2,5-二酮（U73122）。累积地，这项研究表明，通过以磷脂酶C独立的方式释放内质网Ca（2+）并引起Ca（2），芬迪林诱导角膜上皮细胞中浓度依赖性的[Ca（2 +）]（i）增加+）涌入。

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