Dexamethasone-loaded fibroin nanoparticles promote retinal reattachment in rats by regulating the Th17/Treg balance.

Purpose Retinal detachment (RD) is a common acute blinding eye disease. DEX, an adrenocorticosteroid drug, has predominant protective effects on RD. However, given its poor water solubility and low bioavailability, we aimed to develop an alternative nano-based treatment approach to investigate the effects and underlying mechanisms of RD. Methods SF@DEX nanomaterials were synthesized and then successfully characterized. In vitro, phagocytosis was measured by flow cytometry. The expression levels of IL-17 and IL-10 were determined by ELISA. A rat model of RD was established by surgery. Then, rats were orally administered with SF, SF@DEX, and DEX, respectively. The level of IL-17A and FOXP3 was assessed by PCR, and the expression levels of TGF-β1, IL-10, IL-17A, and FOXP3 were detected by Western blot. The apoptotic level of retinal ganglion cells (RGCs) in retinal tissue was measured by TUNEL assay, and confocal microscopy was used to detect changes in the colocalization content of IL-17A and FOXP3 in retinal tissue. Results Our results demonstrated that the nanoparticles exhibited good stability. The encapsulation efficiency (EE) was 90%, and approximately 60% of DEX was released within 12 hours from the dialysis bag. In vivo, after treatment with SF@DEX, the expression of Th17 cells and IL-17A significantly decreased, while the expression levels of Tregs, FOXP3, TGF-β1, and IL-10 were increased. Furthermore, SF@DEX nanomaterial treatment markedly alleviated the severity of RD in rats. Conclusion Taken together, these findings demonstrate that SF@DEX can protect against RD and inhibit inflammation, mediated by regulating the Th17/Treg immune balance. .