Helium preconditioning protects against neonatal hypoxia-ischemia via nitric oxide mediated up-regulation of antioxidases in a rat model
Helium preconditioning protects against neonatal hypoxia-ischemia via nitric oxide mediated up-regulation of antioxidases in a rat model
复制标题
氦气预处理通过大鼠模型中一氧化氮介导的抗氧化酶上调防止新生儿缺氧缺血
DOI：
10.1016/j.bbr.2015.12.001
复制
发表时间：
2016-03-01
影响因子：
2.7
通讯作者：
Mao, Y. F.
中科院分区：
文献类型：
--
作者：
Li, Y.;Liu, K.;Mao, Y. F.
本研究旨在探讨一氧化氮（NO）在氦预处理（He-PC）对新生大鼠缺氧缺血（HI）神经保护作用中的作用。7日龄大鼠随机分为正常对照组、He-PC组、HI组、He-PC+HI组、L-NAME+HI组和L-NAME + He-PC+ HI组。HI通过暴露于80%氧气90 min诱导。He-PC用70%氦气-30%氧气进行3次5 min。He-PC组和对照组于注射后3 h处死动物，取脑组织测定NO含量。HI后24 h处死对照组、HI组、He-PC+HI组、L-NAME+He-PC+HI组动物，取脑检测梗死率、抗氧化酶（SOD、HO-1、Nrf 2）、Nrf 2 DNA结合活性及TUNEL染色。3周后测定神经功能和脑萎缩情况。结果表明，单独应用L-NAME预处理对HI无保护作用。He PC可显著增加NO含量，缩小脑梗死面积，增加抗氧化酶表达和Nrf 2 DNA结合活性，减少凋亡细胞，改善神经功能和脑萎缩。此外，这种保护作用被L-NAME（一种非选择性NOS抑制剂）显著抑制。提示He-PC可能通过诱导NO产生激活Nrf 2，对新生儿HI具有神经保护作用。(C)2015爱思唯尔B. V.保留所有权利。
This study aimed to investigate the role of nitric oxide (NO) in the neuroprotective effects of helium preconditioning (He-PC) in a neonatal hypoxia/ischemia (HI) rat model. Seven-day old rat pups were divided into normal control group, He-PC group, HI group, He-PC+HI group, L-NAME+HI group and L NAME + He-PC+ HI group. HI was induced by exposure to 80% oxygen for 90 min. He-PC was conducted with 70% helium-30% oxygen for three 5-min periods. Three hours after He-PC, animals in control group and He-PC group were sacrificed, and the brain was collected for the detection of NO content. At 24 h after HI, animals in control group, HI group, He-PC+HI group, and L-NAME+He-PC+HI group were sacrificed, and the brain was collected for detection of infarct ratio, antioxidases (SOD, HO-1 and Nrf2), DNA binding activity of Nrf2 and TUNEL staining. Three weeks later, the neurological function and brain atrophy were determined. Results showed pretreatment with L-NAME alone failed to exert protective effect on HI. He PC significantly increased NO content, reduced the brain infarct area, increased anti-oxidases expression and DNA binding activity of Nrf2, decreased the apoptotic cells, and improved the neurological function and brain atrophy. In addition, this protection was markedly inhibited by L-NAME (a non-selective NOS inhibitor). These findings suggest that the He-PC may induce NO production to activate Nrf2, exerting neuroprotective effect on neonatal HI. (C) 2015 Elsevier B.V. All rights reserved.