Protective effect of Bufei Yishen Formula against cigarette smoke extract-induced human bronchial epithelial cell damage and its mechanism.
10.12122/j.issn.1673-4254.2025.07.03
- Author:
Zhengyuan FAN
1
;
Zihan SHEN
2
;
Ya LI
1
;
Tingting SHEN
1
;
Gaofeng LI
2
;
Suyun LI
3
Author Information
1. Chinese Medicine Pharmacology (Respiratory) Laboratory, Henan Key Laboratory of Traditional Chinese Medicine for Respiratory Disease Prevention and Treatment, First Affiliated Hospital of Henan University of Chinese Medicine, Zhengzhou 450000, China.
2. Henan Province and Ministry of Education Co-construction Collaborative Innovation Center for Chinese Medicine and Respiratory Diseases, Henan University of Chinese Medicine, Zhengzhou 450046, China.
3. Department of Respiratory Medicine, First Affiliated Hospital of Henan University of Chinese Medicine, Zhengzhou 450000, China.
- Publication Type:Journal Article
- Keywords:
Bufei Yishen Formula;
TLR4/NF‑κB signaling pathway;
cigarette smoke extract;
inflammation response;
mucin hypersecretion
- MeSH:
Humans;
Epithelial Cells/cytology*;
Drugs, Chinese Herbal/pharmacology*;
NF-kappa B/metabolism*;
Bronchi/cytology*;
Smoke/adverse effects*;
Apoptosis/drug effects*;
Mucin 5AC/metabolism*;
Cell Line;
Toll-Like Receptor 4/metabolism*;
Mucin-5B/metabolism*;
Signal Transduction/drug effects*;
Nicotiana;
Rats;
Thiocarbamates/pharmacology*;
Animals
- From:
Journal of Southern Medical University
2025;45(7):1372-1379
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVES:To evaluate the protective effect of Bufei Yishen Formula (BYF) against cigarette smoke extract (CSE)-induced injuries in human bronchial epithelial BEAS-2B cells and explore the underlying mechanism.
METHODS:BEAS-2B cells exposed to CSE were treated with normal rat serum, BYF-medicated rat serum at low or high doses, pyrrolidine dithiocarbamate (PDTC, a NF-κB inhibitor), PDTC combined with high-dose BYF-medicated serum, or S-carbomethyloysteine (S-CMC, as the positive control). CCK-8 assay was used to determine the optimal concentration and treatment time of CSE, BYF-medicated serum and S-CMC. The treated cells were examined for inflammatory factor levels in the supernatant and cellular expressions of MUC5AC and MUC5B using ELISA, cell ultrastructural changes with transmission electron microscopy, and cell apoptosis rate using flow cytometry. The expression levels of TLR4/NF‑κB pathway-associated mRNAs and proteins were determined by qRT-PCR and Western blotting.
RESULTS:CSE exposure significantly increased secretions of IL-1β, IL-6 and TNF-α, mRNA and protein expressions of MUC5AC and MUC5B, and early and total apoptosis rates in BEAS-2B cells, where the presence of apoptotic bodies was detected. CSE also significantly enhanced the mRNA and protein expressions of TLR4, I-κB, and NF-κB and reduced mRNA and protein expressions of AQP5. Treatments of the CSE-exposed cells with BYF-medicated serum, PDTC and S-CMC all significantly lowered inflammatory factor levels, MUC5AC and MUC5B expressions, and early and total cell apoptosis rates, and partly reversed the changes in cellular ultrastructure and mRNA and protein expressions of the TLR4/NF-κB pathway, and the effects were the most conspicuous following the combined treatment with high-dose BYF-medicated serum and PDTC.
CONCLUSIONS:BYF can inhibit cell apoptosis, inflammation and mucus hypersecretion in CSE-induced BEAS-2B cells by inhibiting the TLR4/NF-κB signaling pathway.
