Miralles de Imperial-Ollero Juan A, Gallego-Ortega Alejandro, Ortín-Martínez Arturo, Villegas-Pérez María Paz, Valiente-Soriano Francisco J, Vidal-Sanz Manuel
Departamento de Oftalmología, Universidad de Murcia e Instituto Murciano de Investigación Biosanitaria (IMIB) Virgen de la Arrixaca, Campus de CC de la Salud, El Palmar, 30120 Murcia, Spain.
Donald K. Johnson Eye Institute, Krembil Research Institute, University Health Network, Toronto, ON M5T 2S8, Canada.
Life (Basel). 2021 Oct 26;11(11):1137. doi: 10.3390/life11111137.
Phototoxicity animal models have been largely studied due to their degenerative communalities with human pathologies, e.g., age-related macular degeneration (AMD). Studies have documented not only the effects of white light exposure, but also other wavelengths using LEDs, such as blue or green light. Recently, a blue LED-induced phototoxicity (LIP) model has been developed that causes focal damage in the outer layers of the superior-temporal region of the retina in rodents. In vivo studies described a progressive reduction in retinal thickness that affected the most extensively the photoreceptor layer. Functionally, a transient reduction in a- and b-wave amplitude of the ERG response was observed. Ex vivo studies showed a progressive reduction of cones and an involvement of retinal pigment epithelium cells in the area of the lesion and, in parallel, an activation of microglial cells that perfectly circumscribe the damage in the outer retinal layer. The use of neuroprotective strategies such as intravitreal administration of trophic factors, e.g., basic fibroblast growth factor (bFGF), brain-derived neurotrophic factor (BDNF), ciliary neurotrophic factor (CNTF) or pigment epithelium-derived factor (PEDF) and topical administration of the selective alpha-2 agonist (Brimonidine) have demonstrated to increase the survival of the cone population after LIP.
由于光毒性动物模型与人类病理学(如年龄相关性黄斑变性,AMD)存在退行性共性,因此对其进行了大量研究。研究不仅记录了白光照射的影响,还记录了使用发光二极管(LED)的其他波长(如蓝光或绿光)的影响。最近,已经开发出一种蓝光发光二极管诱导的光毒性(LIP)模型,该模型会在啮齿动物视网膜颞上区域的外层造成局灶性损伤。体内研究描述了视网膜厚度的逐渐减少,其中光感受器层受影响最广泛。在功能上,观察到视网膜电图(ERG)反应的a波和b波振幅短暂降低。体外研究表明,视锥细胞逐渐减少,病变区域的视网膜色素上皮细胞参与其中,同时,小胶质细胞被激活,完美地界定了视网膜外层的损伤范围。使用神经保护策略,如玻璃体内注射营养因子,如碱性成纤维细胞生长因子(bFGF)、脑源性神经营养因子(BDNF)、睫状神经营养因子(CNTF)或色素上皮衍生因子(PEDF),以及局部应用选择性α-2激动剂(溴莫尼定),已证明可增加LIP后视锥细胞群体的存活率。