Effect of thymol on Ca super(2+ homeostasis and viability in human glioblastoma cells)

The effect of the natural essential oil thymol on cytosolic Ca super(2+ concentrations ([Ca) super(2)+] sub(i) and viability in human glioblastoma cells was examined. The Ca) super(2)+-sensitive fluorescent dye fura-2 was applied to measure [Ca super(2+]) sub(i). Thymol at concentrations of 400-1000...

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Veröffentlicht in:European journal of pharmacology 2011-11, Vol.670 (1), p.85-91
Hauptverfasser: Hsu, Shu-Shong, Lin, Ko-Long, Chou, Chiang-Ting, Chiang, An-Jen, Liang, Wei-Zhe, Chang, Hong-Tai, Tsai, Jeng-Yu, Liao, Wei-Chuan, Huang, Fong-Dee, Huang, Jong Khing, Chen, I-Shu, Liu, Shuih-Inn, Kuo, Chun-Chi, Jan, Chung-Ren
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container_issue 1
container_start_page 85
container_title European journal of pharmacology
container_volume 670
creator Hsu, Shu-Shong
Lin, Ko-Long
Chou, Chiang-Ting
Chiang, An-Jen
Liang, Wei-Zhe
Chang, Hong-Tai
Tsai, Jeng-Yu
Liao, Wei-Chuan
Huang, Fong-Dee
Huang, Jong Khing
Chen, I-Shu
Liu, Shuih-Inn
Kuo, Chun-Chi
Jan, Chung-Ren
description The effect of the natural essential oil thymol on cytosolic Ca super(2+ concentrations ([Ca) super(2)+] sub(i) and viability in human glioblastoma cells was examined. The Ca) super(2)+-sensitive fluorescent dye fura-2 was applied to measure [Ca super(2+]) sub(i). Thymol at concentrations of 400-1000 mu M induced a [Ca super(2+]) sub(i) rise in a concentration-dependent fashion. The response was decreased partially by removal of extracellular Ca super(2+. Thymol-induced Ca) super(2)+ signal was not altered by nifedipine, econazole, SK&F96365, and protein kinase C activator phorbol myristate acetate (PMA), but was inhibited by the protein kinase C inhibitor GF109203X. When extracellular Ca super(2+ was removed, incubation with the endoplasmic reticulum Ca) super(2)+ pump inhibitor thapsigargin or 2,5-di-tert-butylhydroquinone (BHQ) abolished thymol-induced [Ca super(2+]) sub(i) rise. Incubation with thymol also abolished thapsigargin or BHQ-induced [Ca super(2+]) sub(i) rise. Inhibition of phospholipase C with U73122 abolished thymol-induced [Ca super(2+]) sub(i) rise. At concentrations of 200-800 mu M, thymol killed cells in a concentration-dependent manner. This cytotoxic effect was not changed by chelating cytosolic Ca super(2+ with 1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid/acetoxy methyl (BAPTA/AM). Annexin V/propidium iodide staining data suggest that thymol (200, 400 and 600 mu M) induced apoptosis in a concentration-dependent manner. Collectively, in human glioblastoma cells, thymol induced a [Ca) super(2)+] sub(i rise by inducing phospholipase C- and protein kinase C-dependent Ca) super(2)+ release from the endoplasmic reticulum and Ca super(2+ entry via non store-operated Ca) super(2)+ channels. Thymol induced cell death that may involve apoptosis.
doi_str_mv 10.1016/j.ejphar.2011.08.017
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The Ca) super(2)+-sensitive fluorescent dye fura-2 was applied to measure [Ca super(2+]) sub(i). Thymol at concentrations of 400-1000 mu M induced a [Ca super(2+]) sub(i) rise in a concentration-dependent fashion. The response was decreased partially by removal of extracellular Ca super(2+. Thymol-induced Ca) super(2)+ signal was not altered by nifedipine, econazole, SK&amp;F96365, and protein kinase C activator phorbol myristate acetate (PMA), but was inhibited by the protein kinase C inhibitor GF109203X. When extracellular Ca super(2+ was removed, incubation with the endoplasmic reticulum Ca) super(2)+ pump inhibitor thapsigargin or 2,5-di-tert-butylhydroquinone (BHQ) abolished thymol-induced [Ca super(2+]) sub(i) rise. Incubation with thymol also abolished thapsigargin or BHQ-induced [Ca super(2+]) sub(i) rise. Inhibition of phospholipase C with U73122 abolished thymol-induced [Ca super(2+]) sub(i) rise. At concentrations of 200-800 mu M, thymol killed cells in a concentration-dependent manner. This cytotoxic effect was not changed by chelating cytosolic Ca super(2+ with 1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid/acetoxy methyl (BAPTA/AM). Annexin V/propidium iodide staining data suggest that thymol (200, 400 and 600 mu M) induced apoptosis in a concentration-dependent manner. Collectively, in human glioblastoma cells, thymol induced a [Ca) super(2)+] sub(i rise by inducing phospholipase C- and protein kinase C-dependent Ca) super(2)+ release from the endoplasmic reticulum and Ca super(2+ entry via non store-operated Ca) super(2)+ channels. 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The Ca) super(2)+-sensitive fluorescent dye fura-2 was applied to measure [Ca super(2+]) sub(i). Thymol at concentrations of 400-1000 mu M induced a [Ca super(2+]) sub(i) rise in a concentration-dependent fashion. The response was decreased partially by removal of extracellular Ca super(2+. Thymol-induced Ca) super(2)+ signal was not altered by nifedipine, econazole, SK&amp;F96365, and protein kinase C activator phorbol myristate acetate (PMA), but was inhibited by the protein kinase C inhibitor GF109203X. When extracellular Ca super(2+ was removed, incubation with the endoplasmic reticulum Ca) super(2)+ pump inhibitor thapsigargin or 2,5-di-tert-butylhydroquinone (BHQ) abolished thymol-induced [Ca super(2+]) sub(i) rise. Incubation with thymol also abolished thapsigargin or BHQ-induced [Ca super(2+]) sub(i) rise. Inhibition of phospholipase C with U73122 abolished thymol-induced [Ca super(2+]) sub(i) rise. 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The Ca) super(2)+-sensitive fluorescent dye fura-2 was applied to measure [Ca super(2+]) sub(i). Thymol at concentrations of 400-1000 mu M induced a [Ca super(2+]) sub(i) rise in a concentration-dependent fashion. The response was decreased partially by removal of extracellular Ca super(2+. Thymol-induced Ca) super(2)+ signal was not altered by nifedipine, econazole, SK&amp;F96365, and protein kinase C activator phorbol myristate acetate (PMA), but was inhibited by the protein kinase C inhibitor GF109203X. When extracellular Ca super(2+ was removed, incubation with the endoplasmic reticulum Ca) super(2)+ pump inhibitor thapsigargin or 2,5-di-tert-butylhydroquinone (BHQ) abolished thymol-induced [Ca super(2+]) sub(i) rise. Incubation with thymol also abolished thapsigargin or BHQ-induced [Ca super(2+]) sub(i) rise. Inhibition of phospholipase C with U73122 abolished thymol-induced [Ca super(2+]) sub(i) rise. At concentrations of 200-800 mu M, thymol killed cells in a concentration-dependent manner. This cytotoxic effect was not changed by chelating cytosolic Ca super(2+ with 1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid/acetoxy methyl (BAPTA/AM). Annexin V/propidium iodide staining data suggest that thymol (200, 400 and 600 mu M) induced apoptosis in a concentration-dependent manner. Collectively, in human glioblastoma cells, thymol induced a [Ca) super(2)+] sub(i rise by inducing phospholipase C- and protein kinase C-dependent Ca) super(2)+ release from the endoplasmic reticulum and Ca super(2+ entry via non store-operated Ca) super(2)+ channels. Thymol induced cell death that may involve apoptosis.</abstract><doi>10.1016/j.ejphar.2011.08.017</doi></addata></record>
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subjects 12-O-Tetradecanoylphorbol-13-acetate
Annexin V
Apoptosis
Ca super(2+)-transporting ATPase
Calcium
Calcium (extracellular)
Calcium channels
Calcium homeostasis
Calcium influx
Endoplasmic reticulum
Essential oils
Fura-2
glioblastoma cells
Phorbol esters
Phospholipase C
propidium iodide
Protein kinase C
thapsigargin
thymol
title Effect of thymol on Ca super(2+ homeostasis and viability in human glioblastoma cells)
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