Sodium hydrosulfide prevents hypoxia-induced behavioral impairment in neonatal mice
Sodium hydrosulfide prevents hypoxia-induced behavioral impairment in neonatal mice
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硫氢化钠可预防新生小鼠缺氧引起的行为障碍
DOI：
10.1016/j.brainres.2013.09.043
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发表时间：
2013-11
期刊：
影响因子：
2.9
通讯作者：
Liu Dexiang
中科院分区：
文献类型：
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作者：
Gu Jianhua;Xie Kai;Zhang Qingrui;Liu Dexiang
新生儿缺氧性脑病是新生儿癫痫发作和长期神经系统异常的常见原因。内源性硫化氢（H2S）在脑内可能具有多种功能。本研究的目的是调查是否硫氢化钠（NaHS），H2S供体，对新生儿缺氧诱导的神经行为缺陷提供保护。新生小鼠在出生后第1天进行缺氧（5%氧气120 min），并接受NaHS（5.6 mg/kg）每日1次，连续3d。于缺氧后3-30 d检测神经行为毒性。用NaHS治疗显著减弱了由缺氧诱导的感觉和运动反射的延迟发展，直到损伤后两周。此外，在低氧30 d后，Morris水迷宫实验显示NaHS可改善低氧动物的学习记忆能力。在暴露于缺氧的小鼠中，用NaHS处理增强海马中脑源性神经营养因子（BDNF）的表达。此外，NaHS的保护作用与其抑制小鼠脑海马缺氧诱导的一氧化氮合酶（NOS）活性和一氧化氮产生的能力有关。两者合计，这些结果表明，持久的有益效果NaHS对缺氧诱导的神经行为缺陷介导的，至少部分，诱导BDNF表达和抑制NOS活性在小鼠的大脑。
Hypoxic encephalopathy is a common cause of neonatal seizures and long-term neurological abnormalities. Endogenous hydrogen sulfide (H2S) may have multiple functions in brain. The aim of this study is to investigate whether sodium hydrosulfide (NaHS), a H2S donor, provides protection against neonatal hypoxia-induced neurobehavioral deficits. Neonatal mice were subjected to hypoxia (5% oxygen for 120 min) at postnatal day 1 and received NaHS (5.6 mg/kg) once daily for 3 d. Neurobehavioral toxicity was examined at 3–30 d after hypoxia. Treatment with NaHS significantly attenuated the delayed development of sensory and motor reflexes induced by hypoxia up to two weeks after the insult. Moreover, NaHS improved the learning and memory performance of hypoxic animals as indicated in Morris water maze test at 30 d after hypoxia. In mice exposed to hypoxia, treatment with NaHS enhanced expression of brain derived neurotrophic factor (BDNF) in the hippocampus. Furthermore, the protective effects of NaHS were associated with its ability to repress the hypoxia-induced nitric oxide synthase (NOS) activity and nitric oxide production in the hippocampus of mice brain. Taken together, these results suggest that the long-lasting beneficial effects of NaHS on hypoxia-induced neurobehavioral deficits are mediated, at least in part, by inducing BDNF expression and suppressing NOS activity in the brain of mice.
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DOI：
10.1523/jneurosci.16-03-01066.1996
发表时间：
1996-02
期刊：
--
影响因子：
--
作者：
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通讯作者：
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DOI：
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期刊：
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影响因子：
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