Astaxanthin ameliorates allergic rhinitis via suppression of the HMGB1/TLR4 signaling pathway.

INTRODUCTION

Allergic rhinitis (AR) is a common inflammatory disease of the nasal mucosa mediated by immunoglobulin E (IgE). Astaxanthin (AST) has been demonstrated to attenuate airway inflammation in an asthmatic mouse model. Nonetheless, the precise effect of AST on AR symptoms and the associated mechanism remain unclear.

MATERIAL AND

METHODS

A mouse AR model was established by ovalbumin (OVA) sensitization and challenge, and AST was administered to AR mice. Human nasal epithelial cells (HNEpCs) were stimulated with recombinant human IL-13 to mimic the AR microenvironment in vitro. Hematoxylin-eosin staining was performed for mouse nasal mucosa histologic analysis. The CCK-8 assay was used to evaluate AST cytotoxicity to HNEpCs. ELISA was employed to determine levels of histamine, OVA-specific IgE, and inflammatory mediators. Oxidative stress-related markers were estimated using corresponding assay kits. Western blotting was implemented to estimate oxidative stress- and HMGB1/TLR4 signaling-related protein levels.

RESULTS

AST administration alleviated nasal symptoms, including sneezing and nasal rubbing, in OVA-triggered AR mice. AST mitigated nasal mucosa pathological damage, reduced histamine, OVA-specific IgE, and inflammatory mediators in the serum, and alleviated oxidative stress in the nasal mucosa of AR mice. AST blocked HMGB1/TLR4/NF-κB signaling transduction in both the nasal mucosa of AR mice and IL-13-treated HNEpCs. AST or TAK-242 (a TLR4 inhibitor) ameliorated inflammatory response and oxidative stress in IL-13-stimulated HNEpCs.

CONCLUSIONS

AST treatment ameliorates AR by reducing inflammation and oxidative stress via the HMGB1/TLR4/NF-κB pathway.