Huang Tzu-Lun, 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 2Institute of Medical Sciences, Tzu Chi University, Hualien, Taiwan.
Department of Dermatology, Kaohsiung Medical University Hospital, Kaohsiung, Taiwan 4Department of Dermatology, Kaohsiung Medical University, Kaohsiung, Taiwan.
Invest Ophthalmol Vis Sci. 2015 Apr;56(4):2290-6. doi: 10.1167/iovs.14-15999.
We investigated the efficacy of intravitreal injections of anti-VEGF agents in a rat model of anterior ischemic optic neuropathy.
We applied laser-induced photoactivation on the optic nerve head after intravenously administered rose bengal (RB). The rats immediately received an intravitreal injection of either ranibizumab or PBS. The density of retinal ganglion cells (RGCs) was calculated using retrograde FluoroGold labeling. Visual function was assessed by flash visual-evoked potentials (FVEP). We investigated TUNEL assays of the retinal sections and ED1 staining of the optic nerve.
After treatment, the RGC densities in the anti-VEGF-treated rats were not statistically significant different from those of the PBS-treated rats (57.0% vs. 40.0% in the central retinas; 39.8% vs. 33.6% in midperipheral retinas, both P > 0.05). Measurements of FVEP showed no statistically significant differences in preserved latency or amplitude of the P1 wave between anti-VEGF and PBS groups (latency 131 ± 15 ms versus 142 ± 14 ms, P = 0.157; amplitude 34 ± 12 μv versus 41 ± 13 μv, P = 0.423). Assays of TUNEL showed that there was no statistical difference in the number of apoptotic cells in the RGC layers between anti-VEGF and PBS groups (7.0 ± 0.8 cells/high-power field [HPF] versus 7.8 ± 1.3 cells/HPF; P = 0.275). In the optic nerves, we did not observe statistically significant differences in ED1-positive cells/HPF between anti-VEGF and PBS groups (P = 0.675).
Intravitreal injections of anti-VEGF did not have a protective effect in the rat model of anterior ischemic optic neuropathy.
我们研究了玻璃体内注射抗血管内皮生长因子（VEGF）药物在前部缺血性视神经病变大鼠模型中的疗效。
静脉注射孟加拉玫瑰红（RB）后，我们对视神经乳头进行激光诱导光活化。大鼠随即接受玻璃体内注射雷珠单抗或磷酸盐缓冲液（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）评估视觉功能。我们研究了视网膜切片的末端脱氧核苷酸转移酶介导的缺口末端标记（TUNEL）检测以及视神经的ED1染色。
治疗后，抗VEGF治疗组大鼠的RGC密度与PBS治疗组相比无统计学显著差异（中央视网膜分别为57.0%和40.0%；中周边视网膜分别为39.8%和33.6%，P均>0.05）。FVEP测量显示，抗VEGF组和PBS组之间P1波的潜伏期或波幅保留情况无统计学显著差异（潜伏期131±15毫秒对142±14毫秒，P = 0.157；波幅34±12微伏对41±13微伏，P = 0.42）。TUNEL检测显示，抗VEGF组和PBS组RGC层凋亡细胞数量无统计学差异（7.0±0.8个细胞/高倍视野[HPF]对7.8±1.3个细胞/HPF；P = 0.275）。在视神经中，抗VEGF组和PBS组之间ED1阳性细胞/HPF无统计学显著差异（P = 0.675）。
玻璃体内注射抗VEGF在前部缺血性视神经病变大鼠模型中没有保护作用。
