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在小鼠视神经挤压模型中,于不同损伤后时间点经玻璃体内联合给予睫状神经营养因子和胶质细胞源性神经营养因子后视网膜神经节细胞的存活及轴突再生

Survival and Axonal Regeneration of Retinal Ganglion Cells in a Mouse Optic Nerve Crush Model After a Cell-Based Intravitreal Co-Administration of Ciliary Neurotrophic Factor and Glial Cell Line-Derived Neurotrophic Factor at Different Post-Lesion Time Points.

作者信息

Hu Yue, Grodzki Lynn Michelle, Bartsch Udo

机构信息

Department of Ophthalmology, Experimental Ophthalmology, University Medical Center Hamburg-Eppendorf, 20246 Hamburg, Germany.

出版信息

Cells. 2025 Apr 28;14(9):643. doi: 10.3390/cells14090643.

Abstract

We recently showed, in a mouse optic nerve crush model, that a sustained cell-based intravitreal administration of ciliary neurotrophic factor (CNTF) and glial cell line-derived neurotrophic factor (GDNF) synergistically slowed the lesion-induced degeneration of retinal ganglion cells (RGCs), resulting in the presence of approximately 35% viable RGCs eight months after the lesion. However, the combinatorial neuroprotective treatment was initiated shortly after the lesion. To mimic a more clinically relevant situation, we co-administered both factors either three or five days after an intraorbital nerve crush when approximately 35% or 57% of the RGCs were degenerated, respectively. Analyses of the retinas at different time points after the lesion consistently revealed the presence of significantly more surviving RGCs in retinas co-treated with CNTF and GDNF than in retinas treated with either factor alone. For example, when the neurotrophic factors were administered five days after the nerve crush and the animals were analyzed two months after the lesion, retinas co-treated with CNTF and GDNF contained approximately 40% of the RGCs present at the start of treatment. In comparison, monotherapy with either CNTF or GDNF protected only about 15% or 10% of the RGCs present at baseline, respectively. The number of regenerating axons in the distal nerve stumps was similar in CNTF- and CNTF/GDNF-treated animals, despite the significantly higher number of rescued RGCs in the latter group. These findings have potential implications for studies aimed at developing neuroprotective treatments for optic neuropathies such as glaucoma.

摘要

我们最近在小鼠视神经挤压模型中表明,基于细胞的玻璃体内持续给予睫状神经营养因子(CNTF)和胶质细胞系源性神经营养因子(GDNF)可协同减缓损伤诱导的视网膜神经节细胞(RGCs)变性,导致损伤后八个月约35%的RGCs存活。然而,联合神经保护治疗在损伤后不久就开始了。为了模拟更符合临床实际的情况,我们在眶内神经挤压后三天或五天同时给予这两种因子,此时分别约35%或57%的RGCs已经变性。对损伤后不同时间点的视网膜进行分析,始终显示与单独使用任何一种因子治疗的视网膜相比,联合使用CNTF和GDNF治疗的视网膜中存活的RGCs明显更多。例如,当在神经挤压后五天给予神经营养因子,并且在损伤后两个月对动物进行分析时,联合使用CNTF和GDNF治疗的视网膜中含有治疗开始时约40%的RGCs。相比之下,单独使用CNTF或GDNF进行单一疗法分别仅保护了基线时约15%或10%的RGCs。尽管后者组中挽救的RGCs数量明显更多,但在CNTF和CNTF/GDNF治疗的动物中,远端神经残端的再生轴突数量相似。这些发现对于旨在开发针对青光眼等视神经病变的神经保护治疗的研究具有潜在意义。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ea5e/12071274/66788b95bfbf/cells-14-00643-g001.jpg

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