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首页> 外文期刊>Life sciences >CP55,940 increases intracellular Ca2+ levels in Madin-Darby canine kidney cells.
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CP55,940 increases intracellular Ca2+ levels in Madin-Darby canine kidney cells.

机译：CP55,940可提高Madin-Darby犬肾细胞的细胞内Ca2 +水平。

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摘要

The effect of CP55,940, a presumed CB1/CB2 cannabinoid receptor agonist, on intracellular free Ca2+ levels ([Ca2+]i) in Madin-Darby canine kidney cells was examined by using the fluorescent dye fura-2 as a Ca2+ indicator. CP55,940 (2-50 microM) increased [Ca2+]i concentration-dependently with an EC50 of 8 microM. The [Ca2+]i signal comprised an initial rise and a sustained phase. Extracellular Ca2+ removal decreased the maximum [Ca2+]i signals by 32+/-12%. CP55,940 (20 microM)-induced [Ca2+]i signal was not altered by 5 microM of two cannabinoid receptor antagonists, AM-251 and AM-281. CP55,940 (20 microM)-induced [Ca2+]i increase in Ca2+-free medium was inhibited by 86+/-3% by pretreatment with 1 microM thapsigargin, an endoplasmic reticulum Ca2+ pump inhibitor. Conversely, pretreatment with 20 microM CP55,940 in Ca2+-free medium for 6 min abolished thapsigargin-induced [Ca2+]i increases. CP55,940 (20 microM)-induced intracellular Ca2+ release was not inhibited when inositol 1,4,5-trisphosphate formation was abolished by suppressing phospholipase C with 2 microM U73122. Collectively, this study shows that CP,55940 induced significant [Ca2+]i increases in canine renal tubular cells by releasing stored Ca2+ from the thapsigargin-sensitive pools in an inositol 1,4,5-trisphosphate-independent manner, and also by causing extracellular Ca2+ entry. The CP55,940's action appears to be dissociated from stimulation of cannabinoid receptors.
机译：通过使用荧光染料fura-2作为Ca2 +指示剂，检查了假定的CB1 / CB2大麻素受体激动剂CP55940对Madin-Darby犬肾细胞中细胞内游离Ca2 +水平（[Ca2 +] i）的影响。 CP55,940（2-50 microM）依赖性地增加[Ca2 +] i浓度，EC50为8 microM。 [Ca 2+] i信号包括初始上升和持续阶段。细胞外Ca2 +的去除使最大[Ca2 +] i信号降低了32 +/- 12％。 CP55,940（20 microM）诱导的[Ca2 +] i信号没有被5 microM的两种大麻素受体拮抗剂AM-251和AM-281改变。通过用1 microM thapsigargin（一种内质网Ca2 +泵抑制剂）预处理，CP55,940（20 microM）诱导的[Ca2 +] i在无Ca2 +培养基中的增加被抑制了86 +/- 3％。相反，在不含Ca2 +的培养基中用20 microM CP55,940预处理6分钟可消除thapsigargin诱导的[Ca2 +] i的增加。当通过使用2 microM U73122抑制磷脂酶C消除了肌醇1,4,5-三磷酸的形成时，CP55,940（20 microM）诱导的细胞内Ca2 +释放没有被抑制。总体而言，这项研究表明，CP，55940通过不依赖thapsigargin敏感池以肌醇1,4,5-三磷酸酯的方式释放储存的Ca2 +，并引起细胞外凋亡，从而引起犬肾小管细胞[Ca2 +] i显着增加。 Ca2 +进入。 CP55,940的作用似乎与刺激大麻素受体分离。

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