TY - JOUR
T1 - Systemic semaglutide provides a mild vasoprotective and antineuroinflammatory effect in a rat model of ocular hypertensive glaucoma
AU - Mouhammad, Zaynab A
AU - Rombaut, Anne
AU - Bermúdez, Mariana Yolotzin García
AU - Vohra, Rupali
AU - Tribble, James R
AU - Williams, Pete A
AU - Kolko, Miriam
N1 - © 2025. The Author(s).
PY - 2025/7/1
Y1 - 2025/7/1
N2 - Glaucoma is a neurodegenerative disease affecting retinal ganglion cells (RGCs), with a multifactorial genesis that includes inflammation and vascular dysfunction. Emerging evidence suggests that glucagon-like peptide 1 receptor agonist (GLP-1RAs) may serve as promising neuroprotective agents in glaucoma. In this study, we investigated the neuroprotective potential of the GLP-1RA semaglutide (SEM) in a rat model of ocular hypertension (OHT) induced by paramagnetic bead injections in Brown Norwegian rats. Rats were divided into four cohorts, two normotensive (NT) cohorts, and two OHT cohorts, treated with either SEM or saline (HBSS), which served as control. Systemic SEM or HBSS administration was initiated simultaneously with OHT induction. We observed that SEM administration seemed to delay the increase in intraocular pressure (IOP) associated with OHT. Although SEM administration did not improve RGC survival, it significantly improved astrocytic fractal dimension value and lacunarity. In conclusion, our findings suggest that GLP-1RAs may exert neuroprotective effects by delaying IOP elevation and preventing OHT-induced reactive astrocyte and vascular remodeling. These findings highlight the potential of GLP-1RAs for retinal neuroprotection, but further studies are needed to elucidate their applicability in glaucoma.
AB - Glaucoma is a neurodegenerative disease affecting retinal ganglion cells (RGCs), with a multifactorial genesis that includes inflammation and vascular dysfunction. Emerging evidence suggests that glucagon-like peptide 1 receptor agonist (GLP-1RAs) may serve as promising neuroprotective agents in glaucoma. In this study, we investigated the neuroprotective potential of the GLP-1RA semaglutide (SEM) in a rat model of ocular hypertension (OHT) induced by paramagnetic bead injections in Brown Norwegian rats. Rats were divided into four cohorts, two normotensive (NT) cohorts, and two OHT cohorts, treated with either SEM or saline (HBSS), which served as control. Systemic SEM or HBSS administration was initiated simultaneously with OHT induction. We observed that SEM administration seemed to delay the increase in intraocular pressure (IOP) associated with OHT. Although SEM administration did not improve RGC survival, it significantly improved astrocytic fractal dimension value and lacunarity. In conclusion, our findings suggest that GLP-1RAs may exert neuroprotective effects by delaying IOP elevation and preventing OHT-induced reactive astrocyte and vascular remodeling. These findings highlight the potential of GLP-1RAs for retinal neuroprotection, but further studies are needed to elucidate their applicability in glaucoma.
KW - Animals
KW - Disease Models, Animal
KW - Glaucoma/drug therapy
KW - Retinal Ganglion Cells/drug effects
KW - Neuroprotective Agents/pharmacology
KW - Intraocular Pressure/drug effects
KW - Ocular Hypertension/drug therapy
KW - Male
KW - Glucagon-Like Peptides/pharmacology
KW - Astrocytes/drug effects
KW - Anti-Inflammatory Agents/pharmacology
KW - Rats
KW - Inflammation/pathology
KW - Rats, Inbred BN
KW - Cell Survival/drug effects
KW - Glucagon-Like Peptide 1
UR - http://www.scopus.com/inward/record.url?scp=105009795411&partnerID=8YFLogxK
U2 - 10.1186/s13041-025-01224-8
DO - 10.1186/s13041-025-01224-8
M3 - Journal article
C2 - 40597179
SN - 1756-6606
VL - 18
JO - Molecular brain
JF - Molecular brain
IS - 1
M1 - 54
ER -