长期失重对尾悬吊大鼠视网膜和视神经的影响。
Effect of long-term weightlessness on retina and optic nerve in tail-suspension rats.
作者信息
Zhao Hong-Wei, Zhao Jun, Hu Lian-Na, Liang Jing-Nan, Shi Yuan-Yuan, Nie Chuang, Qiu Chang-Yu, Nan Xin-Shuai, Li Yu-Xin, Gao Fu-Lin, Liu Yi, Dong Yu, Luo Ling
机构信息
Chinese PLA General Hospital, Beijing 100039, China; Department of Ophthalmology, the 306th Hospital of PLA, Beijing 100101, China.
Department of Ophthalmology, the 306th Hospital of PLA, Beijing 100101, China.
出版信息
Int J Ophthalmol. 2016 Jun 18;9(6):825-30. doi: 10.18240/ijo.2016.06.06. eCollection 2016.
AIM
To evaluate the effect of long-term weightlessness on retina and optic nerve in tail-suspension (TS) rats.
METHODS
A stimulated weightlessness model was established by suspending rats' tail. After 12wk, the ultrastructure and the number of optic nerve axons were observed by transmission electron microscope. The number of survival retinal ganglion cells (RGCs) was calculated by fluorescent gold retrograde labeling. Retina cells apoptosis was detected by TUNEL staining. The function of optic nerve and retina was evaluated by the visual evoked potential (VEP) and oscillatory potentials (Ops).
RESULTS
The optic nerve axons were swollen and sparsely aligned, and the lamellar separation and myelin disintegration occurred after 12wk in TS rats. The density of optic nerve axons was 32.23±3.92 (vs 37.43±4.13, P=0.0145), the RGCs density was 1645±46 cells/mm(2) (vs 1867±54 cells/mm(2) P=0.0000), the incidence rate of retinal cells apoptosis was 5.38%±0.53% (vs 4.75%±0.54%, P=0.0238), the amplitude of VEP-P100 was 15.43±2.14 µV (vs 17.67±2.17 µV, P=0.0424), the latency of VEP-P100 was 69.05±5.34ms (vs 62.43±4.87ms P=0.0143) and the sum amplitude of Ops was 81.05±8.34 µV (vs 91.67±10.21 µV, P=0.0280) in TS group and the control group, respectively.
CONCLUSION
Long-term weightlessness can induce the ultrastructural changes and functional depress of the optic nerve, as well as retinal cell damages in TS rats.
目的
评估长期失重对尾部悬吊（TS）大鼠视网膜和视神经的影响。
方法
通过悬吊大鼠尾巴建立模拟失重模型。12周后，用透射电子显微镜观察视神经轴突的超微结构和数量。用荧光金逆行标记法计算存活的视网膜神经节细胞（RGCs）数量。用TUNEL染色检测视网膜细胞凋亡。通过视觉诱发电位（VEP）和振荡电位（Ops）评估视神经和视网膜的功能。
结果
TS大鼠在12周后视神经轴突肿胀且排列稀疏，出现板层分离和髓鞘崩解。TS组和对照组视神经轴突密度分别为32.23±3.92（vs 37.43±4.13，P = 0.0145），RGCs密度分别为1645±46个细胞/mm²（vs 1867±54个细胞/mm²，P = 0.0000），视网膜细胞凋亡发生率分别为5.38%±0.53%（vs 4.75%±0.54%，P = 0.0238），VEP-P100波幅分别为15.43±2.14μV（vs 17.67±2.17μV，P = 0.0424），VEP-P100潜伏期分别为69.05±5.34ms（vs 62.43±4.87ms，P = 0.0143），Ops总波幅分别为81.05±8.34μV（vs 91.67±10.21μV，P = 0.0280）。
结论
长期失重可导致TS大鼠视神经超微结构改变和功能减退，以及视网膜细胞损伤。
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