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A Mouse Model of Retinal Ischemia-Reperfusion Injury Through Elevation of Intraocular Pressure
Published on: July 14, 2016
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Fluoxetine Protects Retinal Ischemic Damage in Mice
Giovanni Luca Romano1,2, Lucia Gozzo1, Oriana Maria Maurel1
1Department of Biomedical and Biotechnological Sciences, Section of Pharmacology, University of Catania, 95100 Catania, Italy.
Pharmaceutics
|May 27, 2023
Summary
Topical fluoxetine (FLX) protects retinal ganglion cells (RGCs) from acute damage in mice. This neuroprotective effect preserves retinal function and reduces inflammation following ischemia/reperfusion injury.
Area of Science:
- Ophthalmology
- Neuroscience
- Pharmacology
Background:
- Acute retinal damage poses a significant threat to vision.
- Ischemia/reperfusion (I/R) injury is a common cause of acute retinal damage.
- Neuroprotective strategies are crucial for preserving retinal function.
Purpose of the Study:
- To investigate the neuroprotective potential of topical ocular fluoxetine (FLX).
- To evaluate FLX's efficacy in a mouse model of acute retinal damage.
- To assess FLX's impact on retinal ganglion cell (RGC) function and inflammation.
Main Methods:
- Acute retinal damage induced via ocular ischemia/reperfusion (I/R) in C57BL/6J mice.
- Assessment of RGC function using pattern electroretinogram (PERG).
- Quantification of retinal inflammatory markers (IL-6, TNF-α, Iba-1, IL-1β, S100β) via Digital Droplet PCR.
Main Results:
- Topical FLX significantly improved PERG amplitude and reduced latency in I/R-injured retinas.
- I/R injury led to a significant increase in retinal inflammatory markers.
- FLX treatment significantly attenuated the expression of these pro-inflammatory markers.
Conclusions:
- Topical FLX demonstrates significant neuroprotective effects against RGC damage.
- FLX treatment effectively preserves retinal function and reduces inflammation post-I/R injury.
- Further research is warranted to explore FLX as a therapeutic agent for retinal degenerative diseases.

