低氧吸入可减少视网膜超氧自由基，促进色素性视网膜炎模型中的锥体细胞功能和存活。
Reduced inspired oxygen decreases retinal superoxide radicals and promotes cone function and survival in a model of retinitis pigmentosa.
机构信息
The Wilmer Eye Institute, Johns Hopkins University School of Medicine, Baltimore, MD, USA.
The Wilmer Eye Institute, Johns Hopkins University School of Medicine, Baltimore, MD, USA.
出版信息
Free Radic Biol Med. 2023 Mar;198:118-122. doi: 10.1016/j.freeradbiomed.2023.01.021. Epub 2023 Feb 1.
Retinitis pigmentosa (RP) is caused by many different mutations that promote the degeneration of rod photoreceptors and have no direct effect on cones. After the majority of rods have died cone photoreceptors begin to slowly degenerate. Oxidative damage contributes to cone cell death and it has been hypothesized that tissue hyperoxia due to reduced oxygen consumption from the loss of rods is what initiates oxidative stress. Herein, we demonstrate in animal models of RP that reduction of retinal hyperoxia by reducing inspired oxygen to continuous breathing of 11% O reduced the generation of superoxide radicals in the retina and preserved cone structure and function. These data indicate that retinal hyperoxia is the initiating event that promotes oxidative damage, loss of cone function, and cone degeneration in the RP retina.
色素性视网膜炎（RP）是由许多不同的突变引起的，这些突变会促进视杆细胞的退化，而对视锥细胞没有直接影响。在大多数视杆细胞死亡后，视锥细胞开始缓慢退化。氧化损伤对视锥细胞死亡有贡献，有人假设由于失去视杆细胞导致的耗氧量减少而导致的组织缺氧是引发氧化应激的原因。在此，我们在 RP 的动物模型中证明，通过将吸入氧气减少到持续呼吸 11%O2 来降低视网膜缺氧，可以减少视网膜中超氧自由基的产生，同时保持视锥细胞的结构和功能。这些数据表明，视网膜缺氧是促进氧化损伤、视锥细胞功能丧失和 RP 视网膜中视锥细胞退化的起始事件。
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