Biyuantong decoction improves chronic rhinosinusitis by inhibiting inflammatory cell adhesion via NF-кB pathway modulation

Ethnopharmacological relevance

Biyuantong decoction (BYT), a traditional Chinese medicinal formulation, has been used for years to treat chronic rhinosinusitis (CRS) with good clinical results. However, the underlying mechanisms of its treatment for CRS remain to be fully elucidated.

Study aim

This research investigates the molecular mechanism by which BYT ameliorates CRS and provide new perspectives for CRS treatment research.

Materials and methods

Clinical research is conducted on CRS patients who underwent surgery, and post-operative treatments and observations were performed. The pathological alterations of CRS were inspected by H&E staining and nasal endoscopy. Flow cytometry and ELISA were employed to measure the levels of inflammatory cells and cytokines in the peripheral blood of CRS patients. The cytotoxic impacts of BYT were assessed by cell viability, cell cycle and apoptosis assays. The effects of BYT on the adhesion and invasion of inflammatory cells to endothelial cells were evaluated by hetero-adhesion and transwell assay. Flow cytometry was employed to analyze the expression of cell adhesion molecules (CAMs) on HUVECs. The effects of BYT on NF-κB signaling pathway was analyzed by Western blot and immunofluorescence staining. The chemical components of BYT was determined by UPLC-HRMS, and network pharmacology analysis was adopted to predict potential targets in the NF-κB pathway.

Results

Clinical samples demonstrated that BYT treatment could effectively alleviate sinus mucosal edema and significantly decreased the recurrence rate after surgery. H&E staining disclosed obvious inflammatory cell infiltration in the sinus mucosa of CRS patients. Flow cytometry and ELISA results indicated that BYT treatment reduced the levels of eosinophils (median decrease 16.21 %) and cytokines in peripheral blood. Cell adhesion and transwell assays manifested that BYT inhibited the adhesion and invasion of U937 cells to TNF-α-induced HUVECs. Moreover, BYT counteracted the TNF-α-induced upregulation of CAMs on endothelial cells. Western blot and immunofluorescence analyses confirmed that BYT reduced the expression of NF-κB-related proteins and hindered the nuclear translocation of NF-κB. Network pharmacology analysis and component identification of BYT further supported the function of its compounds in synergistically modulating NF-κB signaling.

Conclusion

BYT enhances the clinical efficacy of CRS by suppressing inflammatory cell adhesion and infiltration into the nasal mucosa via NF-кB pathway regulation. These findings provide a robust foundation for the clinical application of BYT in CRS treatment and suggest interrupting inflammatory cell adhesion as a potential new approach.