中国神经再生研究(英文版)

中国神经再生研究(英文版) ›› 2019, Vol. 14 ›› Issue (4): 728-734.doi: 10.4103/1673-5374.247481

• 原著:视神经损伤修复保护与再生 • 上一篇    下一篇

自主跑轮运动可延缓视神经部分横断后视网膜的原发性变性

  

  • 出版日期:2019-04-15 发布日期:2019-04-15
  • 基金资助:

    国家自然科学基金(81501091)，广东省自然科学基金(2015A030310201); 广东省医学科研基金(A2015393); 广东省领导人才资金(2013); 大学引进学科人才计划(B14036）; 中国国家基础研究计划（973计划）(2015CB351800); 中央大学基础研究基金(21609101)

Voluntary running delays primary degeneration in rat retinas after partial optic nerve transection

Hong-Ying Li 1, 2 , Xi Hong 1 , Mi Huang 2, 3 , Kwok-Fai So 2, 3, 4   

  1. 1 Department of Anatomy, School of Medicine, Jinan University, Guangzhou, Guangdong Province, China
    2 Guangdong-Hongkong-Macau Institute of CNS Regeneration, Ministry of Education CNS Regeneration Collaborative Joint Laboratory, Jinan University, Guangzhou, Guangdong Province, China
    3 Guangdong Key Laboratory of Brain Function and Diseases, Jinan University, Guangzhou, Guangdong Province, China
    4 Department of Ophthalmology and State Key Laboratory of Brain and Cognitive Sciences, The University of Hong Kong, Hong Kong Special Administrative Region, China
  • Online:2019-04-15 Published:2019-04-15
  • Contact: Hong-Ying Li, PhD, thongying@jnu.edu.cn; Kwok-Fai So, PhD, hrmaskf@hku.hk.
  • Supported by:

    The work was supported by the National Natural Science Foundation of China, No. 81501091 (to HYL), the Natural Science Foundation of Guangdong Province of China, No. 2015A030310201 (to HYL); Medical Scientific Research Foundation of Guangdong Province of China, No. A2015393 (to HYL); the funds of Leading Talents of Guangdong Province of China, No. 2013 (to KFS); Programme of Introducing Talents of Discipline to Universities, No. B14036 (to KFS); the National Basic Research Program of China (973 Program), No. 2015CB351800 (to KFS); the Fundamental Research Funds for the Central Universities, No. 21609101 (to KFS)

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摘要：

目前虽然许多研究对自主跑步动物模型的神经保护进行了研究，但自主跑步是否会延迟原发性或继发性神经退化性病变目前尚不明确。视神经部分横断（PONT）模型是用于研究原发性和继发性视神经变性的有价值的青光眼模型，因为它可以将原发性（主要在上半视网膜）与次要（主要在下半视网膜）的变性区分开。因此，实验比较了完成与未完成自主跑轮运动SD大鼠上下半视网膜神经节细胞（RGC）的存活率。实验还使用Western免疫印迹检测了参与视网膜神经节细胞退化、氧化应激和兴奋性毒性的磷酸化c-Jun N-末端激酶、超氧化物歧化酶2和谷氨酰胺合成酶的表达。结果表明自主跑轮运动可延缓易受原发性退化影响的视网膜神经节细胞的死亡，但不能延缓继发性退化。此外，视神经部分横断后自主跑轮运动降低了谷氨酰胺合成酶的表达，但没有降低磷酸化c-Jun N-末端激酶和超氧化物歧化酶2在上视网膜中的表达表明，自主跑轮运动可下调兴奋性毒性，延缓视神经部分横断后视网膜神经节细胞的原发性变性。

orcid: 0000-0003-4039-4246(Kwok-Fai So)

关键词: 自主跑步, 视神经损伤, 视网膜神经节细胞, 青光眼模型, JNKs, 原发性变性, 继发性变性, 神经再生

Abstract:

Running is believed to be beneficial for human health. Many studies have focused on the neuroprotective effects of voluntary running on animal models. There were both primary and secondary degeneration in neurodegenerative diseases, including glaucoma. However, whether running can delay primary or secondary degeneration or both of them was not clear. Partial optic nerve transection model is a valuable glaucoma model for studying both primary and secondary degeneration because it can separate primary (mainly in the superior retina) from secondary (mainly in the inferior retina) degeneration. Therefore, we compared the survival of retinal ganglion cells between Sprague-Dawley rat runners and non-runners both in the superior and inferior retinas. Excitotoxicity, oxidative stress, and apoptosis are involved in the degeneration of retinal ganglion cells in glaucoma. So we also used western immunoblotting to compare the expression of some proteins involved in apoptosis (phospho-c-Jun N-terminal kinases, p-JNKs), oxidative stress (manganese superoxide dismutase, MnSOD) and excitotoxicity (glutamine synthetase) between runners and non-runners after partial optic nerve transection. Results showed that voluntary running delayed the death of retinal ganglion cells vulnerable to primary degeneration but not those to secondary degeneration. In addition, voluntary running decreased the expression of glutamine synthetase, but not the expression of p-JNKs and MnSOD in the superior retina after partial optic nerve transection. These results illustrated that primary degeneration of retinal ganglion cells might be mainly related with excitotoxicity rather than oxidative stress; and the voluntary running could down-regulate excitotoxicity to delay the primary degeneration of retinal ganglion cells after partial optic nerve transection.

Key words: voluntary running, optic nerve injury, oxidative stress, excitotoxicity, JNKs,  , primary degeneration, secondary degeneration