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].