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Related Concept Videos

Open Angle Glaucoma: Treatment01:27

Open Angle Glaucoma: Treatment

427
In open-angle glaucoma, the iridocorneal angle remains open, but the trabecular meshwork becomes stiff, slowing down the outflow of aqueous humor. This causes a buildup of aqueous humor in the anterior chamber, leading to a sudden increase in intraocular pressure. The treatment for open-angle glaucoma focuses on reducing the elevated intraocular pressure by either decreasing the secretion of aqueous humor or increasing its outflow.
Drugs such as carbonic anhydrase inhibitors, α2- and...
427
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  11. Effect Of Bromfenac On Reducing Neuroinflammation In An Ischemia-reperfusion Glaucoma Model

Effect of Bromfenac on Reducing Neuroinflammation in an Ischemia-Reperfusion Glaucoma Model

Si-Eun Oh1, Jie-Hyun Kim2, Chan-Kee Park2

  • 1Department of Ophthalmology, Bucheon St. Mary's Hospital, College of Medicine, The Catholic University of Korea, Seoul 06591, Republic of Korea.

Cells
|June 26, 2024

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Glutamate and Hypoxia as a Stress Model for the Isolated Perfused Vertebrate Retina
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View abstract on PubMed

Summary
This summary is machine-generated.

Bromfenac reduces neuroinflammation and enhances retinal ganglion cell survival in a glaucoma model. This non-prostaglandin anti-inflammatory drug offers a potential new therapeutic avenue for glaucoma patients.

Area of Science:

  • Ophthalmology
  • Neuroscience
  • Pharmacology

Background:

  • Glaucoma progression is linked to intraocular pressure (IOP) and age, but IOP reduction is insufficient.
  • Neuroinflammation is increasingly recognized as a key factor in glaucoma pathogenesis.
  • Existing treatments do not fully halt glaucoma advancement, necessitating novel therapeutic strategies.

Purpose of the Study:

  • To investigate the anti-inflammatory effects of Bromfenac in a rodent model of glaucoma.
  • To assess Bromfenac's impact on glial activation (microglia and astrocytes) and neuroinflammation markers.
  • To evaluate Bromfenac's neuroprotective effects on retinal ganglion cells (RGCs) and retinal function.

Main Methods:

  • An ischemia-reperfusion (IR) glaucoma model was utilized.
Keywords:
glaucomaneuroinflammationretinal ganglion cells

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  • Western blotting and ELISA assessed Bromfenac's effects on glial cells and inflammatory markers.
  • Immunohistochemistry and electroretinography evaluated glial activation, RGC survival, and retinal function.

    • Main Results:

    • Bromfenac downregulated elevated inflammatory markers (iNOS, COX-2, PGE2-R) and necroptosis markers in astrocytes.
    • Glial activation, indicated by GFAP and Iba-1, was reduced following Bromfenac treatment.
    • Bromfenac administration improved RGC survival and preserved retinal function in the IR glaucoma model.

    Conclusions:

    • Bromfenac effectively mitigates neuroinflammation in an experimental glaucoma model.
    • The drug demonstrates significant neuroprotective effects, enhancing RGC survival and function.
    • Bromfenac represents a promising therapeutic agent for managing glaucoma by targeting neuroinflammation.