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首页> 外文期刊>Toxicology in vitro: an international journal published in association with BIBRA >Effect of capsazepine on cytosolic Ca(2+) levels and proliferation of human prostate cancer cells.
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Effect of capsazepine on cytosolic Ca(2+) levels and proliferation of human prostate cancer cells.

机译：辣椒素对人前列腺癌细胞胞质Ca（2+）水平和增殖的影响。

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摘要

Capsazepine has been widely used as a selective antagonist of vanilloid type 1 receptors; however, its other in vitro effect on most cell types is unknown. In human PC3 prostate cancer cells, the effect of capsazepine on intracellular Ca(2+) concentrations ([Ca(2+)](i)) and cytotoxicity was investigated by using fura-2 and tetrazolium, respectively. Capsazepine caused a rapid rise in [Ca(2+)](i) in a concentration-dependent manner with an EC(50) value of 75 microM. Capsazepine-induced [Ca(2+)](i) rise was reduced by 60% by removal of extracellular Ca(2+), suggesting that the capsazepine-induced [Ca(2+)](i) rise was contributed by extracellular Ca(2+) influx and intracellular Ca(2+). Consistently, the capsazepine (200 microM)-induced [Ca(2+)](i) rise was decreased by La(3+) by half. In Ca(2+)-free medium, thapsigargin, an inhibitor of the endoplasmic reticulum Ca(2+)-ATPase, caused a monophasic [Ca(2+)](i) rise, after which the effect of capsazepine on [Ca(2+)](i) was inhibited by 80%. Conversely, pretreatment with capsazepine partly reduced thapsigargin-induced [Ca(2+)](i) rise. U73122, an inhibitor of phospholipase C, abolished histamine (an inositol 1,4,5-trisphosphate-dependent Ca(2+) mobilizer)-induced, but not capsazepine-induced, [Ca(2+)](i) rise. These findings suggest that in human PC3 prostate cancer cells, capsazepine increases [Ca(2+)](i) by evoking Ca(2+) influx and releasing Ca(2+) from the endoplasmic reticulum via a phospholiase C-independent manner. Overnight incubation with capsazepine (200 microM) killed 37% of cells, which could not be prevented by chelating intracellular Ca(2+) with BAPTA.
机译：辣椒素已被广泛用作类香草素1型受体的选择性拮抗剂;但是，它对大多数细胞类型的其他体外作用尚不清楚。在人PC3前列腺癌细胞中，分别使用fura-2和tetrazolium考察了卡塞平对细胞内Ca（2+）浓度（[Ca（2 +）]（i））和细胞毒性的影响。辣椒素以浓度依赖的方式导致[Ca（2 +）]（i）迅速升高，EC（50）值为75 microM。辣椒素诱导的[Ca（2 +）]（i）上升通过去除细胞外Ca（2+）减少了60％，这表明辣椒素诱导的[Ca（2 +）]（i）上升是由细胞外贡献的Ca（2+）涌入和细胞内Ca（2+）。一致地，辣椒碱（200 microM）诱导[Ca（2 +）]（i）上升被La（3+）减少了一半。在无Ca（2+）的培养基中，thapsigargin，一种内质网Ca（2 +）-ATPase的抑制剂，引起单相[Ca（2 +）]（i）升高，此后辣椒碱对[Ca] （2 +）]（i）被抑制80％。相反，用辣椒碱进行的预处理可部分减少thapsigargin诱导的[Ca（2 +）]（i）升高。 U73122，磷脂酶C的抑制剂，废除组胺（一种肌醇1,4,5-三磷酸依赖性Ca（2+）动员剂）诱导，而不是由卡萨平诱导的[Ca（2 +）]（i）升高。这些发现表明，在人类PC3前列腺癌细胞中，辣椒素通过引起Ca（2+）涌入并通过磷酸化酶C独立方式从内质网释放Ca（2+）来增加[Ca（2 +）]（i）。过夜与辣椒素（200 microM）孵育杀死了37％的细胞，无法通过与BAPTA螯合细胞内Ca（2+）来预防。

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