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鱼藤酮诱导的大鼠视神经损伤和视网膜神经节细胞丢失。

Rotenone-Induced Optic Nerve Damage and Retinal Ganglion Cell Loss in Rats.

机构信息

Product Development Division, Santen Pharmaceutical Co., Ltd., Nara 630-0101, Japan.

Ophthalmology Innovation Center, Santen Pharmaceutical Co., Ltd., Nara 630-0101, Japan.

出版信息

Biomolecules. 2024 Aug 23;14(9):1047. doi: 10.3390/biom14091047.

DOI:10.3390/biom14091047
PMID:39334813
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11430293/
Abstract

Rotenone is a mitochondrial complex I inhibitor that causes retinal degeneration. A study of a rat model of rotenone-induced retinal degeneration suggested that this model is caused by indirect postsynaptic N-methyl-D-aspartate (NMDA) stimulation triggered by oxidative stress-mediated presynaptic intracellular calcium signaling. To elucidate the mechanisms by which rotenone causes axonal degeneration, we investigated morphological changes in optic nerves and the change in retinal ganglion cell (RGC) number in rats. Optic nerves and retinas were collected 3 and 7 days after the intravitreal injection of rotenone. The cross-sections of the optic nerves were subjected to a morphological analysis with axon quantification. The axons and somas of RGCs were analyzed immunohistochemically in retinal flatmounts. In the optic nerve, rotenone induced axonal swelling and degeneration with the incidence of reactive gliosis. Rotenone also significantly reduced axon numbers in the optic nerve. Furthermore, rotenone caused axonal thinning, fragmentation, and beading in RGCs on flatmounts and decreased the number of RGC soma. In conclusion, the intravitreal injection of rotenone in rats induced morphological abnormities with a reduced number of optic nerve axons and RGC axons when the RGC somas were degenerated. These findings help elucidate the pathogenesis of optic neuropathy induced by mitochondrial dysfunction.

摘要

鱼藤酮是一种线粒体复合物 I 抑制剂，可导致视网膜变性。一项关于鱼藤酮诱导的视网膜变性大鼠模型的研究表明，这种模型是由氧化应激介导的突触前细胞内钙信号触发的间接突触后 N-甲基-D-天冬氨酸 (NMDA) 刺激引起的。为了阐明鱼藤酮引起轴突变性的机制，我们研究了大鼠视神经的形态变化和视网膜神经节细胞 (RGC) 数量的变化。在玻璃体内注射鱼藤酮后 3 天和 7 天收集视神经和视网膜。视神经的横截面进行轴突定量的形态分析。在视网膜平面上用免疫组织化学分析 RGC 的轴突和体。在视神经中，鱼藤酮诱导轴突肿胀和变性，并伴有反应性神经胶质增生。鱼藤酮还显著减少了视神经中的轴突数量。此外，鱼藤酮在平面上导致 RGC 的轴突变薄、碎裂和珠状，并减少 RGC 体的数量。总之，在大鼠玻璃体内注射鱼藤酮可诱导视神经形态异常，当 RGC 体发生变性时，视神经轴突和 RGC 轴突数量减少。这些发现有助于阐明由线粒体功能障碍引起的视神经病变的发病机制。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3d0d/11430293/d7105ce79a10/biomolecules-14-01047-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3d0d/11430293/15d480fbff63/biomolecules-14-01047-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3d0d/11430293/2514747e67d4/biomolecules-14-01047-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3d0d/11430293/898d392436a8/biomolecules-14-01047-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3d0d/11430293/f360b38ce13d/biomolecules-14-01047-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3d0d/11430293/d7105ce79a10/biomolecules-14-01047-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3d0d/11430293/15d480fbff63/biomolecules-14-01047-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3d0d/11430293/2514747e67d4/biomolecules-14-01047-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3d0d/11430293/898d392436a8/biomolecules-14-01047-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3d0d/11430293/f360b38ce13d/biomolecules-14-01047-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3d0d/11430293/d7105ce79a10/biomolecules-14-01047-g005.jpg

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本文引用的文献

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Int J Mol Sci. 2022 Jan 30;23(3):1606. doi: 10.3390/ijms23031606.
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MEC17-induced α-tubulin acetylation restores mitochondrial transport function and alleviates axonal injury after intracerebral hemorrhage in mice.MEC17 诱导的α-微管蛋白乙酰化恢复了线粒体运输功能，并减轻了小鼠脑出血后的轴突损伤。
J Neurochem. 2022 Jan;160(1):51-63. doi: 10.1111/jnc.15493. Epub 2021 Aug 31.
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Involvement of endoplasmic reticulum stress in rotenone-induced leber hereditary optic neuropathy model and the discovery of new therapeutic agents.
内质网应激在鱼藤酮诱导的 Leber 遗传性视神经病变模型中的作用及新治疗药物的发现。
J Pharmacol Sci. 2021 Oct;147(2):200-207. doi: 10.1016/j.jphs.2021.07.003. Epub 2021 Jul 22.
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Glial cells modulate retinal cell survival in rotenone-induced neural degeneration.神经退行性变中神经胶质细胞对视网膜细胞存活的调节作用。
Sci Rep. 2021 May 27;11(1):11159. doi: 10.1038/s41598-021-90604-w.
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Pyrroloquinoline Quinone Inhibits Rotenone-Induced Microglia Inflammation by Enhancing Autophagy.吡咯喹啉醌通过增强自噬来抑制鱼藤酮诱导的小胶质细胞炎症。
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