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Effect of nordihydroguaiaretic acid on intracellular Ca(2+) concentrations in C6 glioma cells.

机译:去甲二氢愈创木酸对C6胶质瘤细胞中细胞内Ca(2+)浓度的影响。

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The effect of nordihydroguaiaretic acid (NDGA) on Ca(2+) signaling in C6 glioma cells has been investigated. NDGA (5-100 microM) increased [Ca(2+)]i concentration-dependently. The [Ca(2+)]i increase comprised an initial rise and an elevated phase over a time period of 4 min. Removal of extracellular Ca(2+) reduced NDGA-induced [Ca(2+)]i signals by 52+/-2%. After incubation of cells with NDGA in Ca(2+)-free medium for 4 min, addition of 3 mM CaCl2 induced a concentration-dependent increase in [Ca(2+)]i. NDGA (100 microM)-induced [Ca(2+)]i increases in Ca(2+)-containing medium was not changed by pretreatment with 10 microM nifedipine or verapamil. In Ca(2+)-free medium, pretreatment with the endoplasmic reticulum Ca(2+) pump inhibitor thapsigargin (1 microM) abolished 100 microM NDGA-induced [Ca(2+)]i increases. Inhibition of phospholipase C with 2 microM U73122 had little effect on 100 microM NDGA-induced Ca(2+) release. Several other lipoxygenase inhibitors had no effect on basal [Ca(2+)]i. Collectively, the results suggest that NDGA increased [Ca(2+)]i in glioma cells in a lipoxygenase-independent manner, by releasing Ca(2+) from the endoplasmic reticulum in a manner independent of phospholipase C activity and by causing Ca(2+) influx.
机译:已经研究了去甲二氢愈创木酸(NDGA)对C6胶质瘤细胞Ca(2+)信号传导的影响。 NDGA(5-100 microM)浓度依赖性地增加[Ca(2 +)] i。 [Ca(2 +)] i的增加包括4分钟时间的初始上升和上升阶段。去除细胞外Ca(2+)减少NDGA诱导的[Ca(2 +)] i信号52 +/- 2%。细胞与NDGA在无Ca(2+)的培养基中孵育4分钟后,添加3 mM CaCl2诱导[Ca(2 +)] i的浓度依赖性增加。 NDGA(100 microM)诱导[Ca(2 +)] i在含Ca(2+)的培养基中的增加未通过用10 microM硝苯地平或维拉帕米进行预处理而改变。在无Ca(2+)的介质中,使用内质网Ca(2+)泵抑制剂thapsigargin(1 microM)进行的预处理消除了100 microM NDGA诱导的[Ca(2 +)] i。用2 microM U73122抑制磷脂酶C对100 microM NDGA诱导的Ca(2+)释放几乎没有影响。其他几种脂氧合酶抑制剂对基础[Ca(2 +)] i没有影响。总体而言,结果表明NDGA以独立于脂氧合酶的方式通过从内质网释放Ca(2+)并以不依赖磷脂酶C的方式释放Ca(2+)并引起Ca( 2+)涌入。

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