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首页> 外文期刊>Life sciences >Mechanisms of nordihydroguaiaretic acid-induced (Ca2+)i increases in MDCK cells.
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Mechanisms of nordihydroguaiaretic acid-induced (Ca2+)i increases in MDCK cells.

机译：去甲二氢愈创木酸诱导的（Ca2 +）i在MDCK细胞中增加的机制。

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摘要

The effect of nordihydroguaiaretic acid (NDGA), a lipoxygenase inhibitor, on Ca2+ signaling in Madin Darby canine kidney (MDCK) cells has been investigated. NDGA (10-100 microM) increased [Ca2+]i concentration-dependently. The [Ca2+]i increase comprised an initial slow rise and a plateau over a time period of 5 min. Ca2+ removal partly inhibited the Ca2+ signals induced by 25-100 microM NDGA and abolished that induced by 10 microM NDGA. In Ca(2+)-free medium, pretreatment with 0.1 mM NDGA for 12 min abolished the [Ca2+]i increase induced by the mitochondrial uncoupler carbonylcyanide m-chlorophenylhydrazone (CCCP; 2 microM) and the endoplasmic reticulum (ER) Ca2+ pump inhibitor thapsigargin (1 microM). However, 0.1 mM NDGA still increased [Ca2+]i after Ca2+ stores had been depleted by pretreating with 2 microM CCCP, 1 microM thapsigargin and 0.1 mM cyclopiazonic acid. NDGA (50 microM) activated Mn2+ quench of fura-2 fluorescence at 360 nm excitation wavelength, which was almost abolished by 50 microM La3+. This implies NDGA induced Ca2+ influx mainly via a La(3+)-sensitive pathway. Consistently, 50 microM La3+ pretreatment inhibited 0.1 mM NDGA-induced [Ca2+]i increase. Adding 3 mM Ca2+ increased [Ca2+]i in cells pretreated with 0.1 mM NDGA in Ca(2+)-free medium, suggesting NDGA activated capacitative Ca2+ entry. Pretreatment with 0.1 mM NDGA for 200 s prior to Ca2+ did not alter 1 microM thapsigargin-induced capacitative Ca2+ entry. Pretreatment with 40 microM aristolochic acid to inhibit phospholipase A2 reduced 0.1 mM NDGA-induced Ca2+ release by 65%, but inhibiting phospholipase C with 2 microM U73122 had little effect. This suggests NDGA-induced Ca2+ release was independent of inositol 1,4,5-trisphosphate (IP3), but was modulated by phospholipase A2.
机译：脂质过氧化酶抑制剂去甲二氢愈创木酸（NDGA）对Madin Darby犬肾（MDCK）细胞中Ca2 +信号转导的影响已得到研究。 NDGA（10-100 microM）浓度依赖性地增加[Ca2 +] i。 [Ca 2+] i的增加包括初始缓慢上升和在5分钟内的平稳期。 Ca2 +的去除部分抑制了25-100 microM NDGA诱导的Ca2 +信号，而废除了10 microM NDGA诱导的Ca2 +信号。在无Ca（2+）的培养基中，用0.1 mM NDGA预处理12分钟消除了由线粒体解偶联剂羰基氰化物间氯苯hydr（CCCP; 2 microM）和内质网（ER）Ca2 +泵抑制剂引起的[Ca2 +] i增加thapsigargin（1 microM）。但是，在用2 microM CCCP，1 microM thapsigargin和0.1 mM环吡嗪酸预处理Ca2 +储存后，0.1 mM NDGA仍会增加[Ca2 +] i。 NDGA（50 microM）在360 nm激发波长下激活了fura-2荧光的Mn2 +猝灭，几乎被50 microM La3 +消除了。这意味着NDGA主要通过La（3+）敏感途径诱导Ca2 +流入。一致地，50 microM La3 +预处理抑制了0.1 mM NDGA诱导的[Ca2 +] i增加。在不含Ca（2+）的培养基中添加0.1 mM NDGA预处理的细胞中，添加3 mM Ca2 +可以增加[Ca2 +] i，这表明NDGA激活了电容性Ca2 +进入。在加入Ca2 +之前，用0.1 mM NDGA预处理200 s不会改变1 microM毒胡萝卜素诱导的Ca2 +电容进入。用40 microM马兜铃酸进行预处理以抑制磷脂酶A2使0.1 mM NDGA诱导的Ca2 +释放降低了65％，但用2 microM U73122抑制磷脂酶C的作用很小。这表明NDGA诱导的Ca2 +释放独立于肌醇1,4,5-三磷酸（IP3），但受磷脂酶A2调节。

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