PDF(Pubmed)
Abstract：
In the context of glaucoma, intraocular pressure (IOP) and age are recognized as the primary factors contributing to its onset and progression. However, significant reductions in IOP fail to completely halt its advancement. An emerging body of literature highlights the role of neuroinflammation in glaucoma. This study aimed to explore Bromfenac\'s anti-inflammatory properties in mitigating neuroinflammation associated with glaucoma using an ischemia-reperfusion (IR) glaucoma model. Bromfenac\'s impact on microglia and astrocytes under pressure was assessed via Western blotting and an enzyme-linked immunosorbent assay. Immunohistochemical staining was used to evaluate glial activation and changes in inflammatory marker expression in the IR model. Bromfenac led to the downregulation of inflammatory markers, which were elevated in the conditions of elevated pressure, and necroptosis markers were downregulated in astrocytes. In the IR model, elevated levels of GFAP and Iba-1 indicated glial activation. Following Bromfenac administration, levels of iNOS, COX-2, and PGE2-R were reduced, suggesting a decrease in neuroinflammation. Furthermore, Bromfenac administration in the IR model resulted in the improved survival of retinal ganglion cells (RGCs) and preservation of retinal function, as demonstrated by immunohistochemical staining and electroretinography. In summary, Bromfenac proved effective in diminishing neuroinflammation and resulted in enhanced RGC survival.
摘要：
在青光眼的背景下，眼内压(IOP)和年龄是导致其发病和进展的主要因素.然而,IOP的显著降低未能完全阻止其进步。新兴的文献强调了神经炎症在青光眼中的作用。本研究旨在利用缺血再灌注(IR)青光眼模型探讨溴芬酸在缓解与青光眼相关的神经炎症中的抗炎特性。通过蛋白质印迹和酶联免疫吸附测定评估了在压力下溴芬酸对小胶质细胞和星形胶质细胞的影响。免疫组织化学染色用于评估IR模型中神经胶质活化和炎症标志物表达的变化。溴芬酸导致炎症标志物的下调，在高压条件下升高，星形胶质细胞中的坏死标记物下调。在IR模型中，GFAP和Iba-1水平升高表明神经胶质激活。溴芬酸给药后,iNOS的水平，COX-2和PGE2-R降低,表明神经炎症的减少。此外，在IR模型中给予溴芬酸导致视网膜神经节细胞(RGCs)的存活改善和视网膜功能的保存,如免疫组织化学染色和视网膜电图所示。总之,溴芬酸被证明可有效减少神经炎症，并提高RGC的存活率。
