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首页> 外文期刊>Human and Experimental Toxicology >Mechanisms of resveratrol-induced changes in cytosolic free calcium ion concentrations and cell viability in OC2 human oral cancer cells
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Mechanisms of resveratrol-induced changes in cytosolic free calcium ion concentrations and cell viability in OC2 human oral cancer cells

机译：白藜芦醇诱导OC2人口腔癌细胞中胞质游离钙离子浓度和细胞活力变化的机制

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Resveratrol is a natural compound that affects cellular calcium (Ca2+) homeostasis and viability in different cells. This study examined the effect of resveratrol on cytosolic free Ca2+ concentrations ([Ca2+](i)) and viability in OC2 human oral cancer cells. The Ca2+-sensitive fluorescent dye fura-2 was used to measure [Ca2+](i), and water-soluble tetrazolium-I was used to measure viability. Resveratrol evoked concentration-dependent increase in [Ca2+](i). The response was reduced by removing extracellular Ca2+. Resveratrol also caused manganese-induced fura-2 fluorescence quench. Resveratrol-evoked Ca2+ entry was inhibited by nifedipine and the protein kinase C (PKC) inhibitor GFI09203X but was not altered by econazole, SKF96365, and the PKC activator phorbol 12-myristate 13 acetate. In Ca2+-free medium, treatment with the endoplasmic reticulum Ca2+ pump inhibitor 2,5-di-tert-butylhydroquinone (BHQ) abolished resveratrol-evoked [Ca2+](i) rise. Conversely, treatment with resveratrol inhibited BHQ-evoked [Ca2+](i) rise. Inhibition of phospholipase C (PLC) with U73122 abolished resveratrol-evoked [Ca2+](i) rise. At 20-100 mu M, resveratrol decreased cell viability, which was not affected by chelating cytosolic Ca(2+)with 1,2-bis(2-amino-phenoxy)ethane-N,N,N',N'-tetraacetic acid-acetoxymethyl ester. Annexin V-fluorescein isothiocyanate staining data suggest that resveratrol at 20-40 mu M induced apoptosis in a concentration-dependent manner. Collectively, in OC2 cells, resveratrol induced [Ca2+](i) rise by evoking PLC-dependent Ca2+ release from the endoplasmic reticulum and by causing Ca2+ entry via nifedipine-sensitive, PKC-regulated mechanisms. Resveratrol also caused Ca2+-independent apoptosis.
机译：白藜芦醇是一种天然化合物，可影响细胞钙（Ca2 +）的稳态和不同细胞的活力。这项研究检查了白藜芦醇对OC2人口腔癌细胞中胞质游离Ca2 +浓度（[Ca2 +]（i））和活力的影响。使用对Ca2 +敏感的荧光染料fura-2来测量[Ca2 +]（i），并使用水溶性四唑鎓I来测量生存力。白藜芦醇引起[Ca2 +]（i）的浓度依赖性增加。通过去除细胞外Ca2 +降低了反应。白藜芦醇还引起锰诱导的fura-2荧光猝灭。硝苯地平和蛋白激酶C（PKC）抑制剂GFI09203X抑制白藜芦醇引起的Ca2 +进入，但益康唑，SKF96365和PKC激活佛波醇12-肉豆蔻酸酯13乙酸酯未改变白藜芦醇引起的Ca2 +进入。在不含Ca2 +的培养基中，使用内质网Ca2 +泵抑制剂2,5-二叔丁基对苯二酚（BHQ）消除了白藜芦醇引起的[Ca2 +]（i）升高。相反，白藜芦醇治疗抑制了BHQ引起的[Ca2 +]（i）升高。用U73122抑制磷脂酶C（PLC）消除了白藜芦醇引起的[Ca2 +]（i）升高。在20-100μM时，白藜芦醇降低了细胞活力，这不受与1,2-双（2-氨基-苯氧基）乙烷-N，N，N'，N'-四乙酸螯合胞质Ca（2+）的影响酸-乙酰氧基甲酯。 Annexin V-荧光素异硫氰酸酯染色数据表明，白藜芦醇在20-40μM时以浓度依赖性方式诱导凋亡。集体地，在OC2细胞中，白藜芦醇通过引起内质网PLC依赖的Ca2 +释放并通过硝苯地平敏感的PKC调节机制引起Ca2 +进入，从而引起[Ca2 +]（i）升高。白藜芦醇还引起非Ca2 +依赖性细胞凋亡。

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