Glabridin Inhibits Growth and Alleviate Inflammation Mediated by Dectin-2 and NLRP3 Inflammasome.

Purpose: The research was used to uncover the mechanism of glabridin in keratitis in anti-fungus and anti-inflammation.

Methods: , RAW 264.7 cells were infected with with incubation of glabridin in different concentrations. Real-time quantitative polymerase chain reaction (RT‑qPCR), Western blot, and enzyme-linked immunosorbent assay (ELISA) were used to assess the inflammatory severe and alternation with the intervention of Dectin-2 siRNA and glabridin. , keratitis mouse models were established by spore intra-stromal injection and treated with glabridin or PBS. And disease scores, inflammatory mediators, and periodic acid-schiff (PAS) staining were exhibited to demonstrate the therapeutic efficiency of glabridin . Morphological interference assay monitored fungal germination. Scanning and transmission electron microscopy were used to observe the growth of fungi.

Results: In RAW 264.7 cells and mouse keratitis models, noncytotoxic 16 μg/mL glabridin showed significant inhibition in the expression of Dectin-2, NLRP3, Caspase-1, IL-1β, and TNF-α after infection, almost similar to the intervention of Dectin-2 siRNA. PAS staining illustrated the reduced hyphal distribution in cornea stroma with glabridin treatment. Glabridin remarkably inhibited growth through delaying germination and disrupting the integrity of the hyphae membrane.

Conclusion: Glabridin plays an anti-inflammatory role in challenge suppression of the Dectin-2 and NLRP3 inflammasome, and plays an anti-fungal role through delaying germination and changing the hyphal integrity.KEY MESSAGESGlabridin plays an anti-inflammatory role in infection of RAW264.7 cells in a concentration-dependent manner and through Dectin-2 mediation.Glabridin decreases fungal distribution and inflammation in mouse keratitis.Glabridin inhibits growth by delaying germination and disrupting cellular structure .