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Resveratrol protects retinal ganglion cells against ischemia induced damage by increasing Opa1 expression.

Abstract
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.
AuthorsYulian Pang, Mengqi Qin, Piaopiao Hu, Kaibao Ji, Ruihan Xiao, Nan Sun, Xinghui Pan, Xu Zhang
JournalInternational journal of molecular medicine (Int J Mol Med) Vol. 46 Issue 5 Pg. 1707-1720 (Nov 2020) ISSN: 1791-244X [Electronic] Greece
PMID32901846 (Publication Type: Journal Article)
Chemical References
  • Protective Agents
  • Superoxide Dismutase
  • GTP Phosphohydrolases
  • Opa1 protein, rat
  • Resveratrol
Topics
  • Animals
  • Apoptosis (drug effects)
  • Cell Survival (drug effects)
  • Cells, Cultured
  • Disease Models, Animal
  • Down-Regulation (drug effects)
  • GTP Phosphohydrolases (metabolism)
  • Glaucoma (drug therapy, metabolism)
  • Male
  • Mitochondria (drug effects, metabolism)
  • Protective Agents (pharmacology)
  • Rats
  • Rats, Sprague-Dawley
  • Reperfusion Injury (drug therapy, metabolism)
  • Resveratrol (pharmacology)
  • Retina (drug effects, metabolism)
  • Retinal Ganglion Cells (drug effects, metabolism)
  • Superoxide Dismutase (metabolism)

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