Hesperidin-Loaded Nanoparticles Attenuate Pathological Angiogenesis in Oxygen-Induced Retinopathy by Modulating the...

Area of Science:

• Ophthalmology
• Immunology
• Nanotechnology

Background:

• Retinal neovascularization is driven by inflammation, with microglia playing a key role.
• High-mobility group box 1 (HMGB1) promotes pro-inflammatory M1 microglia, exacerbating retinal damage.
• Shifting microglia from M1 to anti-inflammatory M2 phenotype is a potential therapeutic strategy.

Purpose of the Study:

• To develop a targeted therapy to modulate microglial M1/M2 polarization.
• To suppress pathological angiogenesis and retinal inflammation.
• To offer a novel treatment for retinal neovascularization.

Main Methods:

• Engineered a nanoparticle (H-H@MG1) encapsulating hesperidin and targeting M1 microglia.
• Conducted in vitro studies to assess nanoparticle efficacy on microglial polarization.
• Utilized an oxygen-induced retinopathy mouse model for in vivo validation.

Main Results:

• H-H@MG1 nanoparticles selectively targeted M1 microglia in vitro, inhibiting HMGB1 activation and promoting M2 polarization.
• In vivo studies showed H-H@MG1 rebalanced M1/M2 polarization in the retina.
• Reduced pro-inflammatory cytokines (IL-6, TNF-α) and suppressed pathological angiogenesis.

Conclusions:

• The H-H@MG1 nanodelivery system effectively reshapes the retinal immune microenvironment.
• This strategy shows promise in treating retinal neovascularization by reducing inflammation and angiogenesis.
• Targeting microglial polarization offers a viable therapeutic avenue for neovascular eye diseases.