D3.140 - Xiaoqinglong Decoction Combined with Yupingfeng Powder Alleviates Allergic Rhinitis Complicated with Asthma by Inhibiting B Lymphocyte Activation via JAK2/STAT1/MHC-II signaling pathway
Background
Xiaoqinglong Decoction combined with Yupingfeng Powder (XQLDwYPFP) is a classic traditional Chinese medicine formula for treating Allergic rhinitis (AR) and asthma (AS). Currently, a large number of clinical and basic studies have confirmed that XQLDwYPFP can improve the allergic inflammatory response through immunomodulatory effects. However, the specific underlying regulatory mechanism remains unclear. The objective of this study is to further reveal the molecular mechanism and material basis of efficacy of XQLDwYPFP in treating AR complicated with AS.
Method
An AR complicated with AS mouse model was induced by ovalbumin and aluminum hydroxide. After treatment, nose-scratching and sneezing frequencies were counted. ELISA measured OVA-sIgE in serum. HE, PAS, and chromotropic acid staining observed nasal and lung tissue pathology. Flow cytometry detected Th cell subtypes in lung and spleen. Proteomics analyzed differential protein expression in lung tissue, with GO and KEGG for pathway enrichment. Immunofluorescence examined B lymphocyte activation in nasal and lung tissues. Western blotting and immunohistochemistry detected JAK2/STAT1/MHC-II signaling pathway activation. Molecular docking verified the binding energy between XQLDwYPFP's active ingredients and JAK2 and STAT1.
Results
XQLDwYPFP could significantly improve airway allergic symptoms, inhibit the expression of OVA-sIgE in serum, inhibit goblet cell hyperplasia and eosinophil infiltration in nasal and lung tissues, reduce the proportion of Th2 cells in lung and spleen tissues, and up-regulate the Th1/Th2 ratio. Proteomics revealed that the MHC II-mediated antigen presentation signaling pathway was a key signaling pathway for XQLDwYPFP in treating AR complicated with AS. XQLDwYPFP could significantly reduce the number of activated B lymphocytes in nasal and lung tissues, down-regulate the expression levels of JAK2, p-JAK2, STAT1, p-STAT1, and MHC-II proteins. Its representative components had good binding energy with JAK2 and STAT1 protein molecules.
Conclusion
The active ingredients of XQLDwYPFP can inhibit B lymphocyte activation and correct the Th1/Th2 imbalance by regulating the JAK2/STAT1/MHC-II signaling pathway, thereby alleviating AR complicated with AS, which provides a new modern pharmacological proof for XQLDwYPFP to treat AR complicated with AS.
