Inhibition of Caspase-3 Provides Neuroprotection for Retina Ganglion Cells againts NMDA-induced Exitotoxicity in Wistar Rats Oral Presentation - Observational Study - Resident
Abstract
Introduction & Objectives
Glaucoma is a disorder characterized by the presence of optic neuropathy. Visual impairment in
glaucoma is caused by retinal ganglion cell (RGC) apoptosis associated with N-methyl-D-aspartate
(NMDA)-mediated excitotoxicity. Excitotoxicity causes an increase in calcium in cells as well as
activation of caspase-3. Glaucoma therapy is currently given to reduce intraocular pressure (IOP),
but the damage is still progressing progressively. Hesperidin is known as a neuroprotector that can
suppress calpain overactivation in NMDA-treated retina, thereby reducing the upregulation of TNF-,
an inflammatory cytokine, inhibiting calpain activation by suppressing oxidative stress, and
attenuating caspase-3 activation. The aim of this study to proving the effect of oral Hesperidin on the
expression of caspase-3 Retinal Ganglion Cell in Wistar rats model of NMDA-induced glaucoma.
Methods
Experimental research with post test design only randomized control trial Wistar rats with NMDA
induction were divided into 2 treatment and control groups. The treatment group was given oral
Hesperidin at a dose of 100mg/kg/day while the control group was given Na-CMC 182 mg/kg/day for
3 weeks. Retinal caspase-3 expression was examined by immunohistochemical staining. Data were
collected and processed and then the Mann- Whitney test was performed. (significant p<0.05)
Results
The mean percentage and intensity of RGC caspase-3 expression in the treatment group were 4.29 ±
0.49 it was significantly lower than the control group 6.29 ± 0.95 (p value = 0.003).
Conclusion
Hesperidin provides neuroprotection for RGC againts NMDA- induced exitotoxicity by inhibition of
caspase-3.
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Copyright (c) 2023 Andriati Nadhilah Widyarini, Maharani, Fifin L Rahmi, Trilaksana Nugroho, Arnila Novitasari Saubig, Hermawan Istiadi
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