Immunobiology · 2026
ST2-mediated ERK/JNK/P38/NF-κB signaling: a target of Biminkang mixture in minimal persistent inflammation of allergic rhinitis.
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Sun Meng, Zhang Xiaojing, Meng Wei, Zhang Lifeng, Chen Xiangjing, Zhang Xin, Ning Yunhong, Wang Renzhong
Аннотация
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.
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.