5α-双氢睾酮对前列腺癌LNCaP细胞钙离子移动和细胞生长的影响
Journal Title: Di-er Junyi Daxue Xuebao - Year 2008, Vol 29, Issue 10
Abstract
目的:探讨5α-双氢睾酮(DHT)对前列腺癌LNCaP细胞钙离子移动的影响及其机制。方法:应用Fura-2/AM Ca2+ 荧光探针法结合MiraCal荧光成像系统动态检测DHT刺激以及Ca2+通道阻滞剂干预后LNCaP细胞内钙离子浓度([Ca2+]i)的变化。应用MTT法观察细胞活力,流式细胞仪观察早期细胞凋亡率。结果:DHT浓度为1、10、100和1 000 nmol/L时,能快速诱导[Ca2+]i升高,在20 s~3 min升至峰值。细胞外液无Ca2+时,1 000 nmol/L DHT未能诱导[Ca2+]i升高。细胞膜L-型电压门控Ca2+通道阻滞剂维拉帕米(50 μmol/L)、地尔硫(100 μmol/L)或硝苯地平(5 mmol/L)37℃孵育细胞5 min后,能完全抑制1 000 nmol/L DHT诱导的[Ca2+]i升高。磷脂酶C抑制剂新霉素(1 mmol/L)37℃孵育细胞5 min或兰尼定受体阻滞剂普鲁卡因(50 mmol/L)37℃孵育细胞3 min后,对1 000 nmol/L DHT诱导的[Ca2+]i升高没有影响。1 000 nmol/L DHT作用细胞48 h后,与1 000 nmol/L DHT作用前用维拉帕米预孵细胞相比,细胞光密度(D)值[(0.67±0.10) vs (2.13±0.16))和早期细胞凋亡率[(14.31±2.29)% vs (1.07±0.19)%]差异有统计学意义(P<0.01)。结论:DHT可快速地、剂量依赖性地诱导LNCaP细胞[Ca2+]i升高;DHT诱导的LNCaP细胞[Ca2+]i的升高是通过细胞外Ca2+经细胞膜L-型电压门控Ca2+通道流入细胞内实现的,细胞内贮钙库未释放Ca2+。DHT诱导的LNCaP细胞[Ca2+]i升高促进细胞凋亡、抑制细胞生长。
Authors and Affiliations
Yuan-jie TANG
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