Department of Ophthalmology, Clinical Medicine School, Yangzhou University, Subei People's Hospital of Jiangsu Province, No. 98 Nantong West Road, Yangzhou, Jiangsu, China.
Curr Eye Res. 2012 Dec;37(12):1156-64. doi: 10.3109/02713683.2012.713156. Epub 2012 Aug 20.
To evaluate the effects of intravitreal injection of soluble erythropoietin (EPO) receptor (sEPOR) on photoreceptor cell apoptosis in an animal model of retinal detachment (RD).
Various dosages of sEPOR (2, 20, or 200 ng) were injected into the vitreous cavities of normal rats. Three days after injection, retinal function was measured by flash electroretinography (ERG). On day 7, histopathology and retinal morphology were examined by light and transmission electron microscopy (TEM), respectively. Rat models of RD were successfully established by injection of 1.4% sodium hyaluronate into the subretinal space, followed by immediate injection of phosphate-buffered saline (PBS) or sEPOR into the vitreous cavity. On day 3, photoreceptor cell apoptosis was evaluated using terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL), and caspase-3 activity assayed by Western blotting and immunofluorescence. Light microscopic examination of retinal histopathology was used to determine the thickness of the outer nuclear layer (ONL) 14 days after establishment of RD.
There were no significant differences in the latency and amplitude of maximal a, b and oscillatory potential (OP) wave responses by flash ERG before or 3 days after sEPOR injection (p > 0.05). Retinal tissues showed no obvious pathological changes by either light or transmission electron microscopy. Both Western blotting and immunofluorescence indicated consistent sEPOR enhanced caspase-3 activation aggravated apoptosis of photoreceptor cells in RD rat retinas. On day 14, RD ONLs were thinner, according to increasing dosages of sEPOR.
Intravitreal injection of sEPOR exacerbates photoreceptor cell apoptosis in RD models via activation of caspase-3.
评估玻璃体腔内注射可溶性促红细胞生成素受体（sEPOR）对视网膜脱离（RD）动物模型中光感受器细胞凋亡的影响。
将不同剂量的 sEPOR（2、20 或 200ng）注入正常大鼠的玻璃体腔。注射后 3 天，通过闪光视网膜电图（ERG）测量视网膜功能。第 7 天，通过光镜和透射电镜（TEM）分别观察组织病理学和视网膜形态。通过向视网膜下腔注射 1.4%透明质酸钠，然后立即向玻璃体腔注射磷酸盐缓冲盐水（PBS）或 sEPOR，成功建立 RD 大鼠模型。第 3 天，通过末端脱氧核苷酸转移酶介导的 dUTP 缺口末端标记（TUNEL）评估光感受器细胞凋亡，并通过 Western blot 和免疫荧光法测定半胱氨酸天冬氨酸蛋白酶-3（caspase-3）的活性。建立 RD 后 14 天，通过光镜观察视网膜组织病理学来确定外核层（ONL）的厚度。
sEPOR 注射前后（p＞0.05），闪光 ERG 的最大 a、b 和振荡电位（OP）波的潜伏期和振幅均无明显差异。光镜和透射电镜下均未见视网膜组织有明显的病理改变。Western blot 和免疫荧光均表明，sEPOR 增强了 caspase-3 的激活，加重了 RD 大鼠视网膜光感受器细胞的凋亡。第 14 天，随着 sEPOR 剂量的增加，RD 的 ONL 变薄。
玻璃体腔内注射 sEPOR 通过激活 caspase-3 加重 RD 模型中光感受器细胞的凋亡。
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