Huang Tzu-Lun, Wen Yao-Tseng, Chang Chung-Hsing, Chang Shu-Wen, Lin Kung-Hung, Tsai Rong-Kung
Department of Ophthalmology, Far Eastern Memorial Hospital, Banciao District, New Taipei City, Taiwan 2Department of Electrical Engineering, Yuan-Ze University, Chung-Li, Taoyuan, Taiwan 3Institute of Medical Sciences, Tzu Chi University, Hualien, Taiwan.
Institute of Eye Research, Buddhist Tzu Chi General Hospital, Hualien, Taiwan.
Invest Ophthalmol Vis Sci. 2016 Apr;57(4):1878-84. doi: 10.1167/iovs.15-19023.
To investigate effects of intravitreal injections of triamcinolone acetonide (IVI-TA) at different times in a rodent model of nonarteritic anterior ischemic optic neuropathy (rAION).
After inducing ischemic optic neuropathy, the rats received either IVI-TA (0.32 mg/2 μL) at 1 day (1d-TA), 1 week (7d-TA), 2 weeks (14d-TA), or PBS. The density of retinal ganglion cells (RGCs) was calculated using retrograde Fluorogold labeling. Electrophysiological visual function was assessed by flash visual evoked potentials (FVEPs). Apoptosis assays of the retinal sections and immunohistochemistry of ED1 staining of the optic nerves were performed.
Four weeks postinfarct, the 1d- and 7d-TA groups had significantly rescued RGCs in the central (2160 ± 250 mm(2), P = 0.004; 2050 ± 660, P = 0.008, respectively) and midperipheral retinas (1240 ± 130; 1250 ± 220, respectively, both P = 0.004) compared with those of the PBS-treated rats. Flash visual evoked potentials demonstrated improvements in P1 amplitude (μV) in the 1d- and 7d-TA groups (both P < 0.05). Assays of TUNEL showed a decrease in the number of apoptotic cells in the RGC layers of 1d- and 7d-TA-treated retinas compared with the PBS-treated group (both P = 0.004). Cells ED1-positive were significantly decreased in the optic nerve (ON) of the 1d- and 7d-TA groups compared with the PBS group (P = 0.004 and 0.02, respectively).
Within 1 week postinfarct of rAION, IVI-TA had neuroprotective effects on RGC survival with an increase in the electrophysiological amplitude of VEPs and a decrease in microglial infiltration in the ONs.
在非动脉炎性前部缺血性视神经病变（rAION）的啮齿动物模型中，研究不同时间玻璃体内注射曲安奈德（IVI-TA）的效果。
诱导缺血性视神经病变后，大鼠在第1天（1d-TA组）、第1周（7d-TA组）、第2周（14d-TA组）接受IVI-TA（0.32mg/2μL）注射，或注射磷酸盐缓冲液（PBS）。使用逆行荧光金标记计算视网膜神经节细胞（RGC）的密度。通过闪光视觉诱发电位（FVEP）评估电生理视觉功能。对视网膜切片进行凋亡检测，并对视神经进行ED1染色的免疫组织化学检测。
梗死4周后，与PBS处理的大鼠相比，1d-TA组和7d-TA组在中央视网膜（分别为2160±250mm²，P = 0.004；2050±660，P = 0.008）和中周边视网膜（分别为1240±130；1250±220，P均 = 0.004）显著挽救了RGC。闪光视觉诱发电位显示1d-TA组和7d-TA组的P1波幅（μV）有所改善（均P < 0.05）。TUNEL检测显示，与PBS处理组相比，1d-TA组和7d-TA组处理的视网膜RGC层凋亡细胞数量减少（均P = 0.004）。与PBS组相比，1d-TA组和7d-TA组视神经中ED1阳性细胞显著减少（分别为P = 0.004和0.02）。
在rAION梗死1周内，IVI-TA对RGC存活具有神经保护作用，可增加VEP的电生理波幅，并减少视神经中的小胶质细胞浸润。
