神经保护素妥乐平在缺氧缺血性脑损伤小鼠模型中的作用
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Neuroprotective effects of neurotropin in a mouse model of hypoxic-ischemic brain injury
背景与目的
缺血-缺氧损伤会对多个器官造成有害影响。尤其大脑特别脆弱，一旦受损很难再生。目前，治疗方式非常有限。以前的研究报告了神经妥乐平的神经保护作用，妥乐平是来源于接种了牛痘病毒的兔子的发炎皮肤的非蛋白提取物，它使用外周神经损伤小鼠模型和培养的细胞系。然而，仍不明确神经妥乐平是否可能对脑损伤有保护作用。因而，我们利用小鼠缺氧缺血性脑损伤模型研究了神经妥乐平的神经保护作用及其可能的潜在机制。
方 法
通过左颈总动脉闭塞结合暴露于缺氧环境（8%氧气），在成年雄性C57BL/6小鼠中诱导缺氧缺血性脑损伤。小鼠在诱导缺氧-缺血后立即接受生理盐水或2.4单位的神经妥乐平处理。对存活率、神经功能、梗死体积和炎性细胞因子的表达进行评估。
结 果
与对照组相比，缺氧-缺血损伤后的神经妥乐平组的存活率明显较高(100%对62.5%，p < 0.05)，且神经功能缺损评分较低(1；0–2对3；0–5，中位数；区间，p < 0.05)。神经妥乐平的给药还减少了梗死体积(18.3±5.1%对38.3±7.2%，p < 0.05)和促炎细胞因子的mRNA表达。
结 论
神经妥乐平的后处理可以改善缺氧缺血损伤后的存活率和神经预后。我们的研究结果表明，神经妥乐平通过抑制炎症细胞因子对缺氧缺血性脑损伤具有神经保护作用。
原始文献摘要
Hishiyama S, Kotoda M, Ishiyama T, Mitsui K, Matsukawa T. Neuroprotective effects of neurotropin in a mouse model of hypoxic-ischemic brain injury. J Anesth. 2019 May 21. doi: 10.1007/s00540-019-02655-z. [Epub ahead of print] PubMed PMID: 31115666.
Purpose Ischemic–hypoxic insult leads to detrimental effects on multiple organs. The brain is especially vulnerable, and it is hard to regenerate once damaged. Currently, therapeutic options are very limited. Previous studies have reported neuroprotective effects of neurotropin, a non-protein extract derived from the inflamed skin of rabbits inoculated with vaccinia virus, using a murine model of peripheral nerve injury and cultured cell lines. However, whether neurotropin might have protective effects against brain injuries remains unclear. We, therefore, investigated the neuroprotective effect of neurotropin and possible underlying mechanisms, using a mouse model of hypoxic–ischemic brain injury.
Methods Hypoxic–ischemic brain injury was induced via a combination of the left common carotid artery occlusion and exposure to hypoxic environment (8% oxygen) in adult male C57BL/6 mice. Immediately following induction of hypoxia–ischemia, mice received either saline or 2.4 units of neurotropin. The survival rate, neurological function, infarct volume,and expression of inflammatory cytokines were evaluated.
Results Compared to the control group, the neurotropin group exhibited a significantly higher survival rate (100% vs. 62.5%,p < 0.05) and lower neurological deficit scores (1; 0–2 vs. 3; 0–5, median; range, p < 0.05) after the hypoxic–ischemic insult. The administration of neurotropin also reduced infarct volume (18.3 ± 5.1% vs. 38.3 ± 7.2%, p < 0.05) and mRNA expression of pro-inflammatory cytokines.
Conclusions The post-treatment with neurotropin improved survival and neurological outcomes after hypoxic–ischemic insult. Our results indicate that neurotropin has neuroprotective effects against hypoxic–ischemic brain injury by suppressing pro-inflammatory cytokines.
麻醉学文献进展分享
贵州医科大学高鸿教授课题组
翻译：李美胜 编辑：何幼芹 审校：王贵龙