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首页> 外文期刊>Brain research >Mechanism of hyperbaric oxygen preconditioning in neonatal hypoxia-ischemia rat model.
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Mechanism of hyperbaric oxygen preconditioning in neonatal hypoxia-ischemia rat model.

机译:高压氧预处理在新生儿缺氧缺血大鼠模型中的作用。

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摘要

Hypoxic ischemic (HI) injury in neonates damages brain tissues. We examined the mechanism of hyperbaric oxygen preconditioning (HBO-PC) in neonatal HI rat model. Seven-day-old rat pups were subjected to left common carotid artery ligation and hypoxia (8% oxygen at 37 degrees C) for 90 min. HBO (100% O(2), 2.5 atmospheres absolute for 2.5 h) were administered by placing pups in a chamber 24 h before HI insult. Brain injury was assessed by the survival rate, 2,3,5-triphenyltetrazolium chloride (TTC), Nissl, TUNEL straining and caspase-3,caspase-9 activities after HI. In HBO preconditioned animals, survival rate was increased, infarct ratio was decreased, and the positive stained TUNEL cells were reduced, accompanied by the suppression of caspase-3 and -9 activities. These results indicate that a single HBO-PC appears to provide brain protection against HI insult via inhibition of neuronal apoptosis pathways.
机译:新生儿缺氧缺血(HI)损伤会损害脑组织。我们检查了新生HI大鼠模型中高压氧预处理(HBO-PC)的机制。将7天大的幼崽进行左颈总动脉结扎和缺氧(37摄氏度下8%的氧气)90分钟。 HBO(HI侵害前24小时)将幼崽置于室内,以进行HBO(100%O(2),2.5个大气压,持续2.5 h)。脑损伤通过HI后的存活率,2,3,5-三苯基四唑氯化物(TTC),Nissl,TUNEL应变和caspase-3,caspase-9活性来评估。在HBO预处理的动物中,存活率提高,梗塞率降低,染色阳性的TUNEL细胞减少,并伴有caspase-3和-9活性的抑制。这些结果表明,单个HBO-PC似乎可以通过抑制神经元凋亡途径来提供针对HI损伤的脑保护。

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