Abstract

Summary

This study identifies combined NADPH and N-acetylcysteine (NAC) treatment as a synergistic neuroprotective strategy against glaucomatous retinal ganglion cell (RGC) damage and Müller cell gliosis, acting via p38/MAPK pathway inhibition and reduction of oxidative stress. For lighting and healthcare applications, preserving RGC function is critical since these cells include intrinsically photosensitive subtypes (ipRGCs) essential for circadian entrainment, meaning glaucoma progression may impair non-visual light responses relevant to circadian lighting interventions.
Abstract

Key Findings

  • NADPH treatment decreased phosphorylated p38 (p-p38) levels in RGCs and inhibited gliosis in Müller cells via p38/MAPK (but not JNK/MAPK) pathway suppression.
  • NAC treatment reduced apoptosis, axonal damage, and peroxidation in RGCs in both in vitro (OGD model) and in vivo (chronic ocular hypertensive rat) models.
  • Combination of NADPH and NAC produced the greatest improvement in RGC electrophysiological function and Müller cell gliosis prevention, with synergistic crossover effects on peroxidation inhibition and p38/MAPK pathway suppression compared to either treatment alone.
  • Glaucoma patients showed morphological changes in RGCs and Müller cells with elevated p-p38 and Caspase-3 levels, confirming the pathological relevance of the p38/MAPK and apoptotic pathways.
Categories

Categories

Eye Health & Vision: Investigates retinal ganglion cell neurodegeneration and neuroprotective strategies in glaucoma, directly relevant to retinal health and photoreceptor integrity.
The Science of Light: Examines retinal ganglion cell electrophysiological function and light response modulation, relevant to understanding photoreceptor and RGC biology underlying light detection.
Authors

Author(s)

BJ Smith, CF McHugh, AA Hirano
Publication Date

Publication Year

2023
Citations

Number of Citations

3
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