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LOW-INTENSITY PULSED ULTRASOUND PROTECTS RETINAL GANGLION CELLS FROM GLUTAMATE-INDUCED MITOCHONDRIAL DYSFUNCTION AND NEURONAL INJURY
Zeyuan Wang
Peking University People's Hospital
FENS Forum 2026 (2026)
Barcelona, Spain
Board PS04-08PM-057
Presentation
Date TBA
Board: PS04-08PM-057
Event Information
Poster Board
PS04-08PM-057
Poster
View posterAbstract
Progressive retinal ganglion cell (RGC) degeneration is the pathological hallmark of glaucoma and cannot be fully prevented by intraocular pressure–lowering therapies. Glutamate-induced excitotoxicity is a major contributor to RGC injury, characterized by mitochondrial dysfunction and neuronal structural damage. This study aimed to investigate the neuroprotective effects of low-intensity pulsed ultrasound (LIPUS) in a glutamate-induced RGC injury model. Primary RGCs were isolated and cultured in vitro and exposed to glutamate to induce excitotoxic damage. Cells were treated with low-intensity pulsed ultrasound (1 MHz, 20% duty cycle) at different driving voltages (30, 45 and 65 Vpp). Mitochondrial membrane potential was assessed by JC-1 staining, and neuronal integrity was evaluated by Western blot analysis of the neuronal marker TUJ-1. Glutamate exposure caused a marked loss of mitochondrial membrane potential and a significant reduction in TUJ-1 protein expression, indicating severe mitochondrial impairment and neuronal injury. LIPUS treatment partially reversed these pathological changes in a parameter-dependent manner, preserving mitochondrial membrane potential and restoring TUJ-1 expression compared with glutamate-treated cells. These findings demonstrate that LIPUS confers neuroprotection against glutamate-induced excitotoxic injury in primary RGCs by stabilizing mitochondrial function and maintaining neuronal structural integrity. LIPUS may therefore represent a promising non-invasive neuroprotective strategy for glaucoma
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