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首页> 外文期刊>International journal of developmental neuroscience: the official journal of the International Society for Developmental Neuroscience >Corticosteroid responses following hypoxic preconditioning provide neuroprotection against subsequent hypoxic-ischemic brain injury in the newborn rats
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Corticosteroid responses following hypoxic preconditioning provide neuroprotection against subsequent hypoxic-ischemic brain injury in the newborn rats

机译：缺氧预处理后皮质类固醇反应提供了对新生大鼠随后的缺氧缺血性脑损伤的神经保护作用

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Limited research has evaluated the corticosteroids (CS) response in hypoxic preconditioning (PC) induced neuroprotection against subsequent hypoxic-ischemic (HI) brain injury in newborns. To measure, CS response to hypoxic PC, at postnatal day 6 (P6), rat pups were randomly divided into sham, NoPC (exposure to 21% O2) and PC (exposure to 8% O2 for 3h) groups. In a separate experiment, at P6, rat pups were randomly divided into three groups (sham, NoPC+HI, PC+HI). Rat pups in NoPC+HI and PC+HI groups, respectively had normoxic or hypoxic exposure for 3h at P6 and then had the right carotid artery permanently ligated followed by 140min of hypoxia at P7 (HI). Plasma CS levels were measured at 0.5, 1, 3, 6 and 12h after hypoxic PC and hypoxic PC followed by HI. To investigate whether CS response to hypoxic PC provides neuroprotection against HI, at P6, rat pups were randomly divided into five groups. Fifteen minutes prior to PC or normoxic exposure, rat pups in DMSO+PC+HI and DMSO+NoPC+HI groups received DMSO while in RU486+PC+HI and RU486+NoPC+HI groups received RU486 (glucocorticoid receptor blocker, 60mg/kg) s.c., respectively. Afterwards, rat pups were exposed to normoxia (DMSO+NoPC+HI, RU486+NoPC+HI) or hypoxia (DMSO+PC+HI, RU486+PC+HI) for 3h and then HI 24h later (P7). Rat pups at the corresponding age without any exposure to PC or HI or RU486/DMSO were used as sham. We found that hypoxic PC caused CS surge as well as augmented CS surge and preserved the glucocorticoid feedback regulation after HI. Hypoxic PC reduced HI induced early and delayed brain damage. RU486 partially but significantly inhibited hypoxic PC induced neuroprotection
机译：有限的研究已经评估了缺氧预处理（PC）诱导的Neworns中随后缺氧缺血（HI）脑损伤的神经保护剂的皮质类固醇（CS）反应。为了测量，Cs对缺氧PC的反应，在产后第6天（P6），大鼠幼崽随机分为假，NOPC（暴露于21％O 2 ）和PC（暴露于8％O < INF> 2 3小时）组。在单独的实验中，在P6，大鼠幼犬随机分为三组（假，NOPC + HI，PC + HI）。在NOPC + HI和PC + HI组中的大鼠幼崽分别在P6的常氧或缺氧暴露3小时，然后使右颈动脉永久性连接，然后在P7（HI）下缺氧140分钟。在缺氧PC和缺氧PC之后在0.5,1,3,6和12h下测量血浆Cs水平，然后测量。为了探讨Cs对缺氧PC的反应是否提供神经保护，在P6，大鼠幼犬随机分为五组。在PC或常氧暴露前十五分钟，DMSO + PC + PH + HI和DMSO + NOPC + HI在RU486 + PC + HI和Ru486 + NOPC + HI和Ru486 + NOPC + HI ru486（糖皮质激素受体阻滞剂，60mg / kg ）SC分别。然后，将RAT幼仔暴露于常氧（DMSO + NOPC + HI，RU486 + NOPC + HI）或缺氧（DMSO + PC + HI，RU486 + PC + HI）进行3H，然后在24h后（P7）。在没有任何接触到PC或HI或Ru486 / DMSO的情况下的相应年龄的大鼠幼犬用作假。我们发现缺氧PC引起了CS浪涌以及增强的CS浪涌，并在HI之后保留了糖皮质激素反馈调节。缺氧PC诱导早期和延迟脑损伤。 ru486部分但显着抑制缺氧pc诱导神经保护

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