Abstract

This study aimed to investigate the effects of flavonoid glycoside on mitochondrial dysfunction and inflammatory oxidative stress in macular degeneration. Sixty specific-pathogen-free male Bagg and Albino mice were randomly divided into control, model and flavonoid glycoside. Human retinal pigment epithelium cells ARPE-19 were cultured and treated with dimethyl sulfoxide, sodium iodate and flavonoid glycoside respectively. Fundus fluorescein angiography was used to detect the number of mouse retinal leakage; optical coherence tomography retinal thickness. A wave and B wave were detected by electroretinogram. Hematoxylin and eosin staining was used to observe the morphology of mouse retina; phalloidin, translocase of the outer mitochondrial membrane complex subunit 20 and cyclooxygenase III staining were performed on mouse retinal pigment epithelium cells by immunofluorescence. Adenosine triphosphate content in retinal pigment epithelium cells of mice in each group was detected. Compared with the control mice, the number of retinal leakage points in the model increased, the retinal thickness, A wave and B wave decreased, and the levels of Fas and FasL protein increased significantly. After treatment with flavonoid glycoside, the number of retinal leakage decreased the retinal thickness, A wave and B wave increased, and the levels of Fas and FasL protein decreased significantly. Flavonoid glycoside can significantly improve the mitochondrial dysfunction and inflammatory oxidative stress of retinal pigment epithelium cells and play a good role in protecting macular degeneration.