The acute antinociceptive effect of HBO₂ is mediated by a NO-cyclic GMP-PKG-KATP channel pathway in mice.

The acute antinociceptive effect of HBO₂ is mediated by a NO-cyclic GMP-PKG-KATP channel pathway in mice.
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DOI:
10.1016/j.brainres.2010.10.079
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发表时间:
2011-01-12
期刊:
影响因子:
2.9
通讯作者:
Quock RM
Quock RM
中科院分区:
医学3区
文献类型:
--
作者:
Quock LP;Zhang Y;Chung E;Ohgami Y;Shirachi DY;Quock RM

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先前的研究发现,高压氧(HBO2)产生一种依赖于一氧化氮(NO)的急性抗伤感受作用。本研究旨在确定hbo2诱导的急性抗炎反应是否可能涉及no -环gmp -蛋白激酶g - atp敏感钾(KATP)通道。雄性NIH瑞士小鼠接受5分钟HBO2处理(100%氧气在3.5绝对大气压下),并在接下来的6分钟内使用醋酸腹部收缩试验评估HBO2下的抗炎作用。2-(4-羧基苯基)-4,5-二氢-4,4,5,5-四甲基-1H-咪唑基-1-氧-3-氧化物(羧基ptio, NO清除剂)、1H-[1,2,4]-恶二唑-[4,3-a]喹诺沙林-1- 1)(可溶性鸟酰环化酶抑制剂)、rt -8-(4-氯苯硫基)-鸟苷-3',5'-环单磷硫酸盐(一种蛋白激酶g抑制剂)或格列本脲(一种atp敏感的钾通道抑制剂)预处理均能以剂量依赖的方式拮抗hbo2诱导的急性抗炎反应。这些发现表明,hbo2诱导的急性抗伤性可能是由于no -环gmp -蛋白激酶G-KATP通道通路的激活。
Previous research has found that hyperbaric oxygen (HBO2) produces an acute antinociceptive effect that is dependent on nitric oxide (NO). The present study was undertaken to determine whether HBO2-induced acute antinociception might involve a NO–cyclic GMP–protein kinase G–ATP-sensitive potassium (KATP) channel pathway. Male NIH Swiss mice were subjected to a 5-min HBO2 treatment (100% oxygen at 3.5 absolute atmospheres) and antinociception was assessed over the next 6 min still under HBO2 using the acetic acid abdominal constriction test. Pretreatment with 2-(4-carboxyphenyl)-4,5-dihydro-4,4,5,5-tetramethyl-1H-imidazolyl-1-oxy-3-oxide (carboxy-PTIO, an NO scavenger), 1H-[1,2,4]-oxadiazolo-[4,3-a]quinoxalin-1-one) (a soluble guanylyl cyclase-inhibitor, Rp-8-(4-chlorophenylthio)-guanosine-3',5'-cyclic monophosphorothioate (a protein kinase G-inhibitor) or glibenclamide (an ATP-sensitive potassium channel-inhibitor) all led to antagonism of the HBO2-induced acute antinociception in a dose-dependent manner. These findings suggest that HBO2-induced acute antinociception might be due to activation of a NO–cyclic GMP–protein kinase G–KATP channel pathway.
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