Redox evaluation in sepsis model mice by the in vivo ESR technique using acyl-protected hydroxylamine
Redox evaluation in sepsis model mice by the in vivo ESR technique using acyl-protected hydroxylamine
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使用酰基保护羟胺通过体内 ESR 技术评估脓毒症模型小鼠的氧化还原
DOI：
10.1016/j.freeradbiomed.2013.11.011
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发表时间：
2014
期刊：
影响因子：
--
通讯作者：
Keizo Takeshita
中科院分区：
文献类型：
--
作者：
Shoko Okazaki;Yoko Tachibana;Yukari Koga-Ogawa;Keizo Takeshita
在活体电子自旋共振(ESR)中，波谱是一种非侵入性的技术，可以测量活体实验动物的氧化应激。已经测量了注射氮氧自由基后ESR信号的衰减率，以评估动物的氧化应激，尽管探头的布置也可能影响这一速率。由于在小鼠体内注射1-acetoxy-3-carbamoyl-2，2，5，5-tetramethylpyrrolidine 10分钟后，大多数器官或组织中形成羟胺及其对应的氮氧自由基氧化还原对的探针量几乎是恒定的，因此我们通过静脉注射ACP作为氧化还原探针剂的前体，评价了脂多糖诱导的脓毒症模型小鼠的氧化应激。注射ACP后，活体ESR信号在7-8分钟内升高，然后下降。在脂多糖处理的小鼠中，Thein活体信号的衰减明显慢于健康小鼠，而血液和肝脏中氧化还原探针总量的变化率在这两组之间没有显著差异。ESR成像显示，在内毒素处理的小鼠中，在胸部和上腹部观察到的活体信号衰减缓慢。给予聚乙二醇化超氧化物歧化酶和过氧化氢酶的组合，或一氧化氮合酶的抑制剂，或氯化镓，可取消对脂多糖处理的小鼠衰老的抑制。这些结果表明，内毒素处理的小鼠处于氧化应激状态，与巨噬细胞相关的活性氧物种，如超氧化物和过氧亚硝酸盐，主要参与了氧化应激。
In vivoelectron spin resonance (ESR) spectroscopy is a noninvasive technique that measures the oxidative stress in living experimental animals. The rate of decay of the ESR signal right after an injection of nitroxyl radical has been measured to evaluate the oxidative stress in animals, although the probe’s disposition could also affect this rate. Because the amount of probes forming the redox pair of hydroxyl amine and its corresponding nitroxyl radical was shown to be nearly constant in most organs or tissues 10 min after the injection of 1-acetoxy-3-carbamoyl-2,2,5,5-tetramethylpyrrolidine (ACP) in mice, we evaluated the oxidative stress in sepsis model mice induced by lipopolysaccharide (LPS) by intravenously injecting ACP as a precursor of redox probes. Thein vivoESR signal increased up to 7–8 min after the ACP injection and then decreased. Decay of thein vivosignal in LPS-treated mice was significantly slower than that in healthy mice, whereas no significant difference was observed in the rate of change in the total amount of redox probes in the blood and liver between these groups. ESR imaging showed that thein vivosignals observed at the chest and upper abdomen decayed slowly in LPS-treated mice. Suppression of the decay in LPS-treated mice was canceled by the administration of a combination of pegylated superoxide dismutase and catalase, or an inhibitor of nitric oxide synthase, or gadolinium chloride. These results indicate that the LPS-treated mouse is under oxidative stress and that reactive oxygen species, such as superoxide and peroxynitrite, related to macrophages are mainly involved in the oxidative stress.