Language

English

Publication Date

1-22-2024

Journal

International Journal of Molecular Sciences

DOI

10.3390/ijms25021349

PMID

38279349

PMCID

PMC10816972

PubMedCentral® Posted Date

1-22-2024

PubMedCentral® Full Text Version

Post-print

Abstract

Retinal ischemia plays a vital role in vision-threatening retinal ischemic disorders, such as diabetic retinopathy, age-related macular degeneration, glaucoma, etc. The aim of this study was to investigate the effects of S-allyl L-cysteine (SAC) and its associated therapeutic mechanism. Oxidative stress was induced by administration of 500 μM H2O2 for 24 h; SAC demonstrated a dose-dependent neuroprotective effect with significant cell viability effects at 100 μM, and it concurrently downregulated angiogenesis factor PKM2 and inflammatory biomarker MCP-1. In a Wistar rat model of high intraocular pressure (HIOP)-induced retinal ischemia and reperfusion (I/R), post-administration of 100 μM SAC counteracted the ischemic-associated reduction of ERG b-wave amplitude and fluorogold-labeled RGC reduction. This study supports that SAC could protect against retinal ischemia through its anti-oxidative, anti-angiogenic, anti-inflammatory, and neuroprotective properties.

Keywords

Rats, Animals, Rats, Wistar, Cysteine, Hydrogen Peroxide, Reperfusion Injury, Retinal Diseases, Ischemia, Neuroprotective Agents, Anti-Inflammatory Agents, Glaucoma, S-allyl L-cysteine, retinal pigment epithelium, retinal ganglion cell, pyruvate kinase M2, monocyte chemoattractant protein-1, hydrogen peroxide, oxidative stress, retinal ischemia

Published Open-Access

yes

Share

COinS
 
 

To view the content in your browser, please download Adobe Reader or, alternately,
you may Download the file to your hard drive.

NOTE: The latest versions of Adobe Reader do not support viewing PDF files within Firefox on Mac OS and if you are using a modern (Intel) Mac, there is no official plugin for viewing PDF files within the browser window.