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脑蛋白水解物对视神经挤压大鼠模型的保护作用

Protective effects of cerebrolysin in a rat model of optic nerve crush.

作者信息

Huang Tzu-Lun, Huang Sun-Ping, Chang Chung-Hsing, Lin Kung-Hung, Sheu Min-Muh, Tsai Rong-Kung

机构信息

Department of Ophthalmology, Buddhist Tzu Chi General Hospital, Hualien, Taiwan.

Department of Molecular and Human Genetics, Tzu Chi University, Hualien, Taiwan.

出版信息

Kaohsiung J Med Sci. 2014 Jul;30(7):331-6. doi: 10.1016/j.kjms.2014.02.009. Epub 2014 Apr 3.

DOI:10.1016/j.kjms.2014.02.009
PMID:24924838
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11916025/
Abstract

To investigate the effects of cerebrolysin (Cbl) on optic nerves (ON) and retinal ganglion cells (RGC) in a rat model of ON crush. Rats received intravitreal injection of Cbl (n = 20), intra-ON injection of Cbl (n = 20), intraperitoneal injection (IPI) of Cbl (n = 20), or phosphate buffered saline (PBS; n = 20) every day for 2 weeks after ON crush injury. At 3 weeks post-trauma, RGC density was counted by retrograde labeling with FluoroGold and visual function was assessed by flash visual-evoked potentials. Activities of microglia after insults were quantified by immunohistochemical analysis of the presence of ED1 in the optic nerve. At 3 weeks postcrush, the densities of RGCs in the Cbl-IVI group (1125 ± 166/mm(2)) and in the Cbl-IPI treatment group (1328 ± 119/mm(2)) were significantly higher than those in the PBS group (641 ± 214/mm(2)). The flash visual-evoked potential measurements showed that latency of the P1 wave was significantly shorter in the Cbl-IVI- and Cbl-IPI-treated groups (105 ± 4 ms and 118 ± 26 ms, respectively) than in the PBS-treated group (170 ± 20 ms). However, only Cbl IPI treatment resulted in a significant decrease in the number of ED1-positive cells at the lesion sites of the ON (5 ± 2 cells/vs. 30 ± 4 cells/high-power field in control eyes). Treatment with intra-ON injection of Cbl was harmful to the optic nerve in the crush model. Systemic administration of Cbl had neuroprotective effects on RGC survival and visual function in the optic nerve crush model.

摘要

为研究脑蛋白水解物(Cbl)对大鼠视神经挤压伤模型中视神经(ON)和视网膜神经节细胞(RGC)的影响。视神经挤压伤后,大鼠连续2周每天接受玻璃体内注射Cbl(n = 20)、视神经内注射Cbl(n = 20)、腹腔注射(IPI)Cbl(n = 20)或磷酸盐缓冲盐水(PBS;n = 20)。创伤后3周,通过FluoroGold逆行标记计数RGC密度,并用闪光视觉诱发电位评估视觉功能。通过对视神经中ED1存在情况的免疫组织化学分析定量损伤后小胶质细胞的活性。挤压伤后3周,Cbl-IVI组(1125±166/mm²)和Cbl-IPI治疗组(1328±119/mm²)的RGC密度显著高于PBS组(641±214/mm²)。闪光视觉诱发电位测量显示,Cbl-IVI和Cbl-IPI治疗组的P1波潜伏期(分别为105±4 ms和118±26 ms)显著短于PBS治疗组(170±20 ms)。然而,只有Cbl IPI治疗导致视神经损伤部位ED1阳性细胞数量显著减少(5±2个细胞/高倍视野 vs. 对照眼中30±4个细胞/高倍视野)。在挤压伤模型中,视神经内注射Cbl对神经有害。在视神经挤压伤模型中,全身性给予Cbl对RGC存活和视觉功能具有神经保护作用。

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本文引用的文献

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Sonic hedgehog signaling pathway mediates cerebrolysin-improved neurological function after stroke. sonic hedgehog 信号通路介导脑活素改善中风后的神经功能。
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Cerebrolysin, a mixture of neurotrophic factors induces marked neuroprotection in spinal cord injury following intoxication of engineered nanoparticles from metals.脑活素,一种神经营养因子混合物,在金属工程纳米粒子中毒导致的脊髓损伤后能显著诱导神经保护。
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Superior neuroprotective effects of cerebrolysin in nanoparticle-induced exacerbation of hyperthermia-induced brain pathology.纳米颗粒诱导的高温诱导脑病理加重中脑活素的优越神经保护作用。
CNS Neurol Disord Drug Targets. 2012 Feb;11(1):7-25. doi: 10.2174/187152712799960790.
6
Superior neuroprotective effects of cerebrolysin in heat stroke following chronic intoxication of Cu or Ag engineered nanoparticles. A comparative study with other neuroprotective agents using biochemical and morphological approaches in the rat.脑蛋白水解物对铜或银工程纳米颗粒慢性中毒后中暑的卓越神经保护作用。在大鼠中使用生化和形态学方法与其他神经保护剂的比较研究。
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Cerebrolysin in Alzheimer's disease.脑活素治疗阿尔茨海默病
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8
Chronic administration of the neurotrophic agent cerebrolysin ameliorates the behavioral and morphological changes induced by neonatal ventral hippocampus lesion in a rat model of schizophrenia.慢性给予神经营养剂脑活素可改善精神分裂症大鼠模型中海马腹侧损伤引起的行为和形态学变化。
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Lack of protective effect of local administration of triamcinolone or systemic treatment with methylprednisolone against damages caused by optic nerve crush in rats.局部给予曲安奈德或全身用甲泼尼龙治疗未能预防大鼠视神经钳夹伤造成的损害。
Exp Eye Res. 2011 Feb;92(2):112-9. doi: 10.1016/j.exer.2010.12.008. Epub 2010 Dec 24.