Loss of idiopathic retinal ganglion cells (RGCs) leads to irreversible vision defects and is considered the primary characteristic of
glaucoma. However, effective treatment strategies in terms of RGC neuroprotection remain elusive. In the present study, the protective effects of
resveratrol on RGC apoptosis, and the mechanisms underlying its effects were investigated, with a particular emphasis on the function of
optic atrophy 1 (Opa1). In an
ischemia/reperfusion (I/R) injury model, the notable thinning of the retina, significant apoptosis of RGCs, reduction in Opa1 expression and long Opa1
isoform to short Opa1
isoform ratios (L‑Opa1/S‑Opa1 ratio) were observed, all of which were reversed by
resveratrol administration. Serum deprivation resulted in reductions in R28 cell viability,
superoxide dismutase (SOD) activity, Opa1 expression and induced apoptosis, which were also partially reversed by
resveratrol treatment. To conclude, results from the present study suggest that
resveratrol treatment significantly reduced
retinal damage and RGC apoptosis in I/R injury and serum deprivation models. In addition,
resveratrol reversed the downregulated expression of Opa1 and reduced SOD activity. Mechanistically,
resveratrol influenced mitochondrial dynamics by regulating the L‑Opa1/S‑Opa1 ratio. Therefore, these observations suggest that
resveratrol may exhibit potential as a therapeutic agent for RGC damage in the future.