The Effect of S-Allyl L-Cysteine on Retinal Ischemia: The Contributions of MCP-1 and PKM2 in the Underlying Medicinal Properties

Author:

Chao Windsor Wen-Jin12,Chao Howard Wen-Haur2,Lee Hung-Fu3,Chao Hsiao-Ming456ORCID

Affiliation:

1. Department of Medicine, Aston Medical School, Aston University, Birmingham B4 7ET, UK

2. Department of Science, University of British Columbia, Vancouver, BC V6T 1Z4, Canada

3. Department of Neurosurgery, Cheng Hsin General Hospital, Taipei 11220, Taiwan

4. Department of Chinese Medicine, School of Chinese Medicine, China Medical University, Taichung 40402, Taiwan

5. Department of Medicine, Institute of Pharmacology, School of Medicine, National Yang Ming Chiao Tung University, Taipei 11221, Taiwan

6. Department of Ophthalmology, Shin Kong Wu Ho-Su Memorial Hospital, Taipei 111045, Taiwan

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.

Publisher

MDPI AG

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