The present study demonstrates that brimonidine tartrate, an alpha-2 adrenergic receptor agonist, can prevent photoreceptor cell degeneration and the associated Muller cell degenerative signs in an in vitro model of retinal degeneration and retinal detachment (separation of the neuroretina from the retinal pigment epithelium). Similar to control conditions, brimonidine allowed for the formation of highly structured photoreceptor outer segments, prevented the expression of stress markers in Müller cells and preserved the expression patterns of Muller cell markers of proper cell-cell contact and differentiation. Ultrastructural studies also indicated that brimonidine favored the formation of cell-cell junctions between photoreceptor cells and Müller cells, indicating that this phenomenon is associated with the exertion of the neuroprotective effect. The results suggest that brimonidine compounds may be utilized as an effective therapeutic agent for early and late onset retinal degenerations caused by defects in photoreceptor cells, Müller cells or both, and as an adjuvant to therapeutic success in retinal detachment surgery or macular translocation surgery for age-related macular degeneration.
本研究证明,在视网膜变性和视网膜脱离(神经视网膜与视网膜色素上皮分离)的体外模型中,
酒石酸溴莫尼定(一种α-2
肾上腺素能受体激动剂)可以防止感光细胞变性和相关的Muller细胞变性征象。与对照组的情况相似,
溴莫尼定能形成高度结构化的感光体外节段,防止Müller细胞中应激标记物的表达,并保留了Muller细胞标记物的表达模式,以确保细胞间的正常接触和分化。超微结构研究还表明,
溴莫尼定有利于感光细胞和Müller细胞之间细胞-细胞连接的形成,表明这一现象与神经保护作用的发挥有关。研究结果表明,
溴莫尼定化合物可作为一种有效的治疗药物,用于治疗由感光细胞、Müller细胞或两者缺陷引起的早期和晚期视网膜变性,并可作为视网膜脱离手术或老年性黄斑变性黄斑移位手术治疗成功的辅助药物。