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A hypothesis for treating inflammation and oxidative stress with hydrogen sulfide during age-related macular degeneration

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International Journal of Ophthalmology(English edition) 2018年第5期11卷 881-887页

作者： Akash K George Mahavir Singh rubens petit homme Avisek Majumder Harpal S SANDhu Suresh C Tyagi Eye and Vision Science Laboratory Department of PhysiologyUniversity of Louisville School of Medicine Department of Physiology University of Louisville School of Medicine Department of Biochemistry and Molecular Genetics University of Louisville School of Medicine Department of Ophthalmology and Visual Sciences University of Louisville School of Medicine Kentucky Lions Eye Center University of Louisville School of Medicine

Age-related macular degeneration（AMD） is a leading cause of blindness and is becoming a global crisis since affected people will increase to 288 million by ***,age,diabetes,gender,obesity,hypertension,race,hyperopia,iris-color,smoking,sun-light and pyroptosis have varying roles in AMD,but oxidative stress-induced inflammation remains a significant driver of *** is a unique organ as it contains a remarkable oxygengradient that generates reactive oxygen species（ROS） which upregulates inflammatory *** becomes a source of functional and morphological impairments in retinal pigment epithelium（RPE）,endothelial cells and retinal ganglion *** demonstrated that hydrogen sulfide（H2S） acts as a signaling molecule and that it may treat ***,we propose a novel hypothesis that H2S may restore homeostasis in the eyes thereby reducing damage caused by oxidative injury and *** H_2S has been shown to be a powerful antioxidant because of its free-radicals＇ inhibition properties in addition to its beneficial effects in age-relatedconditions,therefore,patients may benefit from H2S salubrious effects not only by minimizing their oxidant and inflammatory injuries to retina but also by lowering retinal glutamate excitotoxicity.

关键词： eye diseases hydrogen sulfide treatment inflammation macula oxidative stress pyroptosis retinal degeneration

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