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新生大鼠缺氧缺血模型中高压氧预处理的机制

Mechanism of hyperbaric oxygen preconditioning in neonatal hypoxia-ischemia rat model.

作者信息

Li Zhang, Liu Wenwu, Kang Zhimin, Lv Shijun, Han Cuihong, Yun Liu, Sun Xuejun, Zhang John H

机构信息

Department of Pathology, Weifang Medical College, Shandong, 261042, PR China.

出版信息

Brain Res. 2008 Feb 27;1196:151-6. doi: 10.1016/j.brainres.2007.12.039. Epub 2007 Dec 28.

Abstract

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.

摘要

新生儿缺氧缺血性(HI)损伤会损害脑组织。我们在新生HI大鼠模型中研究了高压氧预处理(HBO-PC)的机制。将7日龄的幼鼠进行左侧颈总动脉结扎并在37℃下缺氧(8%氧气)90分钟。在HI损伤前24小时,将幼鼠置于舱室内给予HBO(100% O₂,绝对压力2.5个大气压,持续2.5小时)。HI损伤后,通过存活率、2,3,5-氯化三苯基四氮唑(TTC)、尼氏染色、TUNEL染色以及caspase-3、caspase-9活性来评估脑损伤。在HBO预处理的动物中,存活率提高,梗死率降低,TUNEL阳性染色细胞减少,同时caspase-3和-9活性受到抑制。这些结果表明,单次HBO-PC似乎通过抑制神经元凋亡途径为脑提供针对HI损伤的保护作用。

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