ST2-mediated ERK/JNK/P38/NF-κB signaling: a target of Biminkang mixture in minimal persistent inflammation of allergic rhinitis.

BACKGROUND

Minimal persistent inflammation (MPI) significantly contributes to the recurrence of allergic rhinitis (AR). Although the therapeutic efficacy of Biminkang mixture (BMK) in AR treatment is well-documented, the precise mechanisms underlying its modulation of MPI remain unclear.

METHODS

An MPI mouse model and an interleukin-33 (IL-33)-induced T-helper 2 (Th2) cell model were established. The effects of BMK on nasal mucosa remodeling and inflammation in MPI mice were evaluated using hematoxylin & eosin staining and ELISA. Th2 cell viability was measured using a CCK-8 assay. Western blotting and qRT-PCR were performed to evaluate the effects of BMK on the ST2/ERK/JNK/P38/NF-κB signaling cascade.

RESULTS

Administration of BMK notably mitigated nasal mucosa remodeling and inflammation in MPI mice and markedly inhibited IL-33-induced Th2 cell viability. Moreover, BMK inhibited the activation of the ST2/ERK/JNK/P38/NF-κB signaling cascade, and the inhibit effect of BMK on the ERK/JNK/P38/NF-κB pathway was further enhanced by silencing ST2.

CONCLUSIONS

These findings suggest that BMK effectively alleviates MPI by targeting the ST2-mediated ERK/JNK/P38/NF-κB pathway, thereby inhibiting nasal mucosa remodeling, inflammation, and Th2 cell viability.