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Noninfectious Uveitis Therapy

Long-acting release of fluocinolone acetonide microspheres using electrospray technology for noninfectious uveitis therapy


Intravitreous long-acting drug delivery system offers an excellent alternative to multiple injections for the treatment of noninfectious uveitis (NIU). However, the adverse effects of non-biodegradable intravitreal implants of fluocinolone acetonide (FA), such as postoperative hypotony and secondary injury during removal of the implant matrix, are frequent occurrence to affect patient’s compliance. Herein, biodegradable poly (lactic-co-glycolic acid) (PLGA)-based microspheres (MS) containing fluocinolone acetonide (FA@MS) were prepared using an optimized electrospray technology with a voltage of 10.07 kV and the receiving distance of 9.87 cm. The obtained FA@MS with the average particle size of 2.25 μm possessed the high encapsulation efficiency (94.85%) and drug content (9.48%).

In vitro release demonstrated that FA@MS exhibited sustained release for 30 days, and the release characteristic of FA@MS conformed to the Weibull model. In vivo study in a rabbit NIU model indicated that FA@MS continuously released the drug for at least 28 days in vitreum and progressively decreased inflammation of NIU. Furthermore, the intraocular pressure of rabbits treated with blank MS and FA@MS remained the normal level for 28 days, which demonstrated the favorable biosafety of FA@MS. In conclusion, long-acting release of FA@MS provides a promising formulation for NIU treatment.

HIGHLIGHTS


A biodegradable FA@MS was prepared using the modified electrospray technology for intravitreal administration.

FA@MS exhibited the sustained release characteristics for 30 days in the medium of PBS (pH 7.4) with 0.2% Tween 80.

The pharmacodynamics indicated that FA@MS could be continuously released for at least 28 days in vitreum to treat NIU.

Genetic predisposition, autoimmune response, chronic inflammation, oxidative stress, metabolic syndrome, epigenetic modification, mitochondrial dysfunction, neurodegeneration, endocrine disruption, protein misfolding, cellular senescence, angiogenesis imbalance, lipid peroxidation, cytokine cascade, apoptotic signaling, DNA repair deficit, ion channelopathy, receptor desensitization, fibrosis progression, aberrant autophagy

#GeneticRisk, #Autoimmunity, #Inflammation, #OxidativeStress, #MetabolicSyndrome, #Epigenetics, #MitochondrialHealth, #Neurodegeneration, #EndocrineDisruption, #ProteinMisfolding, #CellularSenescence, #Angiogenesis, #LipidPeroxidation, #CytokineStorm, #Apoptosis, #DNARepair, #Channelopathy, #ReceptorBiology, #Fibrosis, #Autophagy


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