6.5 Retinal protective effect of hydrogen sulfide
I/R injury to the retina is the cause of many retinal vascular diseases, such as diabetic retinopathy (DR), glaucoma, retinal artery occlusion (RAO), etc[171]. It is mainly caused by the generation and accumulation of large amounts of ROS during ischemia and reperfusion, which causes a series of oxidative stress and inflammatory responses that promote irreversible damage to retinal ganglion cells, which may eventually lead to vision loss or even blindness[172]. In a study more than a decade ago, researchers injected an H2S donor (ACS67) into the vitreous humor of rats with retinal I/R injury and subsequently found that ACS67 could regulate GSH levels and inhibit apoptosis of RGC-5 cells induced by oxidative stress, thus exerting a protective effec[173]. Another experiment found that direct inhalation of H2S for pretreatment prior to retinal I/R injury in rats reduced the mortality of RGC[174]. In a 2016 study, it was first proposed that enzymes involved in the generation of H2S and related pathways are activated during retinal IRI and may have the ability to induce retinal neovascularization[175]. In addition, H2S may also protect retinal ganglion cells by inhibiting the production of inflammatory factors, activating signaling pathways involved in mediating protection of mitochondrial function and diastolic vascularity[176-178].