Inhibitory effect of cimifugin on allergic inflammation in bronchial epithelial cells via NF-κB pathway
10.3969/j.issn.1000-484X.2024.03.016
- VernacularTitle:升麻素通过NF-κB通路对支气管上皮细胞过敏性炎症反应的抑制作用
- Author:
Junjie CHEN
1
;
Daowen YANG
Author Information
1. 北京中医药大学,北京 100029
- Keywords:
Cimifugin;
NF-κB signaling;
Inflammatory;
Tight junction;
Allergic asthma
- From:
Chinese Journal of Immunology
2024;40(3):534-539
- CountryChina
- Language:Chinese
-
Abstract:
Objective:To figure out the regulatory role of cimifugin in the inflammatory injury and epithelial barrier function in house dust mite(HDM)-induced human bronchial epithelial cells via NF-κB signaling.Methods:Human bronchial epithelial BEAS-2B cells were divided into blank control(Control)group,HDM group,HDM+cimifugin(0.01 μmol/L)group,HDM+cimifugin(0.1 μmol/L)group,HDM+cimifugin(1 μmol/L)group and positive drug(HDM+Dex)group.Cell viability and apoptosis were respectively estimated by MTT and TUNEL assays.Levels of inflammatory factors in cells were examined by ELISA.Transepithelial electrical resistance(TEER)and FITC-dextran 40 kD(FD-40)flux assessed the permeability of cell monolayers.Nuclear translocation of NF-κB in cells was detected by immunofluorescence assay.Western blot was used to analysis expressions of apoptosis,inflammatory,tight junction and NF-κB signaling-associated proteins.Results:HDM induced viability injury,apoptosis,inflammatory response,epithelial barrier damage and activated NF-κB signaling(all P<0.001)in BEAS-2B cells.Cimifugin treatment dose-dependently inhibited the viability injury(P<0.05),apoptosis(P<0.01),inflammatory response(P<0.05),epithelial barrier damage(P<0.05)and inactivated NF-κB signaling(P<0.05)in BEAS-2B cells exposed to HDM.Conclusion:Cimifugin significantly inhibits HDM-elicited inflammatory injury and epithelial barrier damage in bronchial epithelial cells.This finding may provide novel strategies for the prevention and treatment of allergic asthma.
