Lipoxin A4 (LXA4) Reduces Alkali-Induced Corneal Inflammation and Neovascularization and Upregulates a Repair...

Area of Science:

• Ophthalmology
• Immunology
• Pharmacology

Background:

• Corneal alkali injuries cause severe inflammation and neovascularization.
• Effective treatments for severe corneal chemical injuries remain critical.

Purpose of the Study:

• To investigate the anti-inflammatory and anti-angiogenic effects of Lipoxin A4 (LXA4) in a rat model of severe corneal alkali injury.
• To evaluate LXA4's therapeutic potential for chemical corneal burns.

Main Methods:

• Corneal alkali injury was induced in rats using sodium hydroxide (NaOH).
• Rats received topical LXA4 or vehicle treatment for 14 days.
• Corneal opacity, neovascularization, hyphema, cytokine expression, and immune cell infiltration were assessed.

Main Results:

• LXA4 treatment significantly reduced corneal opacity, neovascularization, and hyphema.
• LXA4 decreased pro-inflammatory cytokines (IL-1β, IL-6) and angiogenic factors (MMP-9, VEGFA).
• LXA4 inhibited neutrophil infiltration and promoted M2 macrophage polarization.

Conclusions:

• LXA4 demonstrates significant anti-inflammatory and anti-angiogenic effects in corneal alkali injury.
• LXA4 acts by reducing leukocyte infiltration, cytokine release, and angiogenic factors, while promoting corneal repair.
• LXA4 shows potential as a therapeutic agent for severe corneal chemical injuries.