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【Stroke】含氢气生理盐水的神经保护作用
本文实现了这一目的.
中文摘要:
含氢气生理盐水对大鼠新生儿脑缺血的神经保护作用
脑缺血缺氧是新生儿脑损伤的重要因素。本研究目的是利用大鼠新生儿脑缺血模型，观察含氢气生理盐水对脑缺血后脑损伤的长期和短期保护作用。采用7天生大鼠，左恻颈总动脉结扎， 8%低氧37 ◦C处理90分钟，制备动物模型。分别在模型制备后即刻和8小时后腹腔注射5 ml/kg饱和氢气生理盐水。24小时后断头处死动物进行TTC、尼氏和TUNEL染色。利用caspase-3活性、MDA和Iba-1免疫组化染色评价细胞死亡、炎症和氧化损伤程度。利用自发活动实验、水迷宫检测5周后神经功能情况。结果发现，氢气生理盐水对能有效降低caspase-3活性、MDA, Iba-1水平、梗死体积，提高长期神经行为功能。氢气生理盐水可能具有治疗新生儿脑缺血等各类脑缺血性疾病的价值。
本文首次证明通过注射含氢盐水可以治疗缺血损伤, 从日本首先发表呼吸2%氢治疗脑缺血的文章以后, 很多研究相继发表,证明呼吸氢可以治疗肝缺血、心肌缺血和小肠移植损伤，通过引用含氢水可以治疗人类糖尿病后氧化损伤，可以治疗应激动导致的脑损伤，可以治疗基因模型动物的脑损伤和动脉硬化。这些研究表明，给一定浓度的氢是一种非常好的治疗氧化损伤的手段。但是，通过注射的方法在临床上将是更理想的给药手段。我们经过反复研究，制备出含氢液体，并用这种注射液治疗脑损伤，效果理想。我们将在其他不同模型中继续证明这种注射液的作用，并深入研究其作用机制。我们相信，本文章的发表将会有力推动氢生物学效应的研究。希望有兴趣的战友加入我们的团队。
我们将来将希望在，缺血、炎症、创伤和各类慢性损伤模型中进行该课题研究，请继续关注我们的工作，我们相信，这些研究将给人类健康带来一个新的希望。氢的系列药物将属于高效、低毒、广谱的治疗药物。
如果将来确实能实现临床应用,本文将具有十分重要的意义.
Neuroprotective Effects of Hydrogen Saline in Neonatal Hypoxia-ischemia Rat Model
[/color]Abstract
Cerebral hypoxia–ischemia (HI) represents a major cause of brain damage in
the term newborn. This study aimed to examine the short and long-term
neuroprotective effect of hydrogen saline (H2 saline) using an established
neonatal HI rat pup model. Seven-day-old rat pups were subjected to left
common carotid artery ligation and then 90 min hypoxia (8% oxygen at 37 ◦C).
H2 saturated saline was administered by peritoneal injection (5 ml/kg)
immediately and again at 8 h after HI insult. At 24 h after HI, the pups were
decapitated and brain morphological injury was assessed by
2,3,5-triphenyltetrazolium chloride (TTC), Nissl, and TUNEL staining. Acute
cell death, inflammation and oxidative stress were evaluated at 24 h by
studying caspase-3 activity, MDA measurement as well as Iba-1
immunochemistry in the brain. At 5 weeks after HI, spontaneous activity test
and Morris water maze test were conducted. We observed that H2 saline
treatment reduced the caspase activity, MDA, Iba-1 levels, the infarct ratio, and
improved the long-term neurological and neurobehavioral functions. H2
saline has potentials in the clinical treatment of HI and other ischemia-related
cerebral diseases.[color=red] 本人已认领该文编译，48小时后若未提交译文，请其他战友自由认领。 全文发布
1. Introduction
Cerebral hypoxia–ischemia (HI) represents a major cause of brain damage in the term newborn. Although the mechanisms involved in HI were not completely understood, neuronal cell death either necrosis or apoptosis may play a critical role (Martin et al., 2000; Northington et al., 2001). Specially, apoptosis represents a treatable target which may occur in penumbra areas for days after the initial insult (Pulera et al., 1998). However, there is no specific treatment which is available to HI patients (Perlman, 2006).
Inflammation and oxidative stress are the two major causes of apoptosis identified after ischemic brain injury including neonatal HI (Kriz, 2006). Microglia was involved in the inflammatory process induced by the HI (Stoll et al., 1998). Allograft inflammatory factor-1 (AIF-1) in microglia is an index for the activation of microglia (Postler etal., 2000). Oxidative stress after HI damages to DNA, membrane and proteins and contribute to apoptotic changes. The malondialdehyde (MDA) is the product of lipid membrane oxidation and a marker of the oxidative damage.
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作者:admin@医学,生命科学 2011-03-10 17:11
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