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首页> 外文期刊>British Journal of Pharmacology >Antioxidant protection of NO-induced relaxations of the mouse anococcygeus against inhibition by superoxide anions, hydroquinone and carboxy-PTIO
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Antioxidant protection of NO-induced relaxations of the mouse anococcygeus against inhibition by superoxide anions, hydroquinone and carboxy-PTIO

机译:抗氧化保护NO诱导的小鼠无球菌松弛不受超氧阴离子,对苯二酚和羧基PTIO的抑制

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摘要

1 The potential protective effect of several antioxidants [Cu/Zn superoxide dismutase (Cu/Zn SOD), ascorbate, reduced glutathione (GSH), and α-tocopherol (α-TOC)] on relaxations of the mouse anococcygeus muscle to nitric oxide (NO; 15 μM) and, where appropriate, nitrergic field stimulation (10 Hz; 10 s trains) was investigated. 2 The superoxide anion generating drug duroquinone (100 μM) reduced relaxations to exogenous NO by 54 ± 6%; this inhibition was partially reversed by Cu/Zn SOD (250 u ml~(-1)), and by ascorbate (500 μM). Following inhibition of endogenous Cu/Zn SOD activity with diethyldithiocarbamate (DETCA), duroquinone (50 μM) also reduced relaxations to nitrergic field stimulation (by 53±6%) and this effect was again reversed by Cu/Zn SOD and by ascorbate. Neither GSH (500 μM) nor α-TOC (400 μM) afforded any protection against duroquinone.
机译:1几种抗氧化剂[Cu / Zn超氧化物歧化酶(Cu / Zn SOD),抗坏血酸,还原型谷胱甘肽(GSH)和α-生育酚(α-TOC)]的潜在保护作用对小鼠无球菌肌肉向一氧化氮的释放具有抑制作用( NO; 15μM),以及在适当时进行的硝化场刺激(10 Hz; 10 s列)。 2产生超氧阴离子的药物duroquinone(100μM)使外源NO的弛豫降低了54±6%;这种抑制作用被Cu / Zn SOD(250 u ml〜(-1))和抗坏血酸盐(500μM)部分逆转。在用二乙基二硫代氨基甲酸酯(DETCA)抑制内源性Cu / Zn SOD活性后,杜洛醌(50μM)也减少了对硝化场刺激的弛豫(降低53±6%),这种作用又被Cu / Zn SOD和抗坏血酸所逆转。 GSH(500μM)和α-TOC(400μM)均未提供针对杜洛醌的保护作用。

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