Huan Yu, Wu Xiu-Quan, Chen Tao, Dou Ya-Nan, Jia Bo, He Xin, Wei Dong-Yu, Fei Zhou, Fei Fei
Department of Neurosurgery, Xijing Hospital, Air Force Medical University, Xi'an, Shaanxi Province, China.
Center of Clinical Aerospace Medicine; Department of Aviation Medicine, Xijing Hospital, Air Force Medical University, Xi'an, Shaanxi Province, China.
Neural Regen Res. 2023 Apr;18(4):922-928. doi: 10.4103/1673-5374.353848.
Retinal injury after blunt ocular trauma may directly affect prognosis and lead to vision loss. To investigate the pathological changes and molecular mechanisms involved in retinal injury after blunt ocular trauma, we established a weight drop injury model of blunt ocular trauma in male Beagle dogs. Hematoxylin-eosin staining, immunofluorescence staining, western blotting, and TUNEL assays were performed to investigate retinal injury within 14 days after blunt ocular trauma. Compared with the control group, the thicknesses of the inner and outer nuclear layers, as well as the number of retinal ganglion cells, gradually decreased within 14 days after injury. The number of bipolar cells in the inner nuclear layer began to decrease 1 day after injury, while the numbers of cholinergic and amacrine cells in the inner nuclear layer did not decrease until 7 days after injury. Moreover, retinal cell necroptosis increased with time after injury; it progressed from the ganglion cell layer to the outer nuclear layer. Visual electrophysiological findings indicated that visual impairment began on the first day after injury and worsened over time. Additionally, blunt ocular trauma induced nerve regeneration and Müller glial hyperplasia; it also resulted in the recruitment of microglia to the retina and polarization of those microglia to the M1 phenotype. These findings suggest that necroptosis plays an important role in exacerbating retinal injury after blunt ocular trauma via gliosis and neuroinflammation. Such a role has important implications for the development of therapeutic strategies.
钝性眼外伤后的视网膜损伤可能直接影响预后并导致视力丧失。为了研究钝性眼外伤后视网膜损伤所涉及的病理变化和分子机制，我们建立了雄性比格犬钝性眼外伤的重物坠落损伤模型。进行苏木精-伊红染色、免疫荧光染色、蛋白质印迹法和TUNEL检测，以研究钝性眼外伤后14天内的视网膜损伤情况。与对照组相比，损伤后14天内内核层和外核层的厚度以及视网膜神经节细胞的数量逐渐减少。内核层中的双极细胞数量在损伤后1天开始减少，而内核层中的胆碱能细胞和无长突细胞数量直到损伤后7天才开始减少。此外，视网膜细胞坏死性凋亡随损伤后的时间增加；它从神经节细胞层发展到外核层。视觉电生理结果表明，视力损害在损伤后第一天开始，并随时间恶化。此外，钝性眼外伤诱导神经再生和Müller胶质细胞增生；它还导致小胶质细胞募集到视网膜并使其极化到M1表型。这些发现表明，坏死性凋亡通过胶质增生和神经炎症在加重钝性眼外伤后的视网膜损伤中起重要作用。这种作用对治疗策略的开发具有重要意义。
