Effect of Shufeng Jiedu Capsules on Relieving Influenza Virus Pneumonia by Suppressing TLR/NF-κB Pathway in Respiratory Epithelial Cells
10.13422/j.cnki.syfjx.20242241
- VernacularTitle:疏风解毒胶囊通过抑制呼吸道上皮细胞TLR/NF-κB通路缓解流感病毒性肺炎
- Author:
Zihan GENG
1
;
Lei BAO
1
;
Shan CAO
1
;
Qiang ZHU
2
;
Jun PAN
2
;
Shuran LI
1
;
Ronghua ZHAO
1
;
Jing SUN
1
;
Yanyan BAO
1
;
Shaoqiu MU
3
;
Xiaolan CUI
1
;
Shanshan GUO
1
Author Information
1. Institute of Chinese Materia Medica China Academy of Chinese Medical Sciences，Beijing 100700，China
2. Anhui Jiren Pharmaceutical Co.Ltd.，Bozhou 230093，China
3. Biological Data of Human （BDHM），Beijing 102488，China
- Publication Type:Journal Article
- Keywords:
Shufeng Jiedu capsules;
influenza A virus H1N1;
respiratory epithelial cell;
Toll-like receptor signaling pathway
- From:
Chinese Journal of Experimental Traditional Medical Formulae
2025;31(24):61-68
- CountryChina
- Language:Chinese
-
Abstract:
ObjectiveTo investigate the possible mechanism of Shufeng Jiedu capsules （SFJD） in alleviating influenza A （H1N1） virus pneumonia and focus on its effect on Toll-like receptor （TLR） signaling pathway in respiratory epithelial cells. MethodsA mouse model of viral pneumonia was established via the A/PR/8/34 （PR8） strain of influenza A virus. Mice were randomly divided into a normal group， a PR8 infection （PR8） group， and an SFJD group （8.4 g·kg-1）， with 10 mice in each group. The day of infection was designated as day 1. The SFJD group was administered intragastrically at a volume of 20 mL·kg-1 daily， while the normal and PR8 groups were given an equal volume of deionized water. Micro-computed tomography （Micro-CT） was performed on day 5， and the mice were dissected to collect their lungs， after which the lung index was calculated to verify the therapeutic effect of SFJD. Single-cell sequencing was used to analyze the differentially expressed genes in respiratory epithelial cells. Multiplex fluorescence immunohistochemistry was employed to detect the expression of TLR， tumor necrosis factor receptor-associated factor 6 （TRAF6）， and myeloid differentiation factor 88 （MyD88） proteins in epithelial cell adhesion molecule （EpCAM）-positive cells， and the proportion of respiratory epithelial cells expressing TLR pathway proteins was calculated. Respiratory epithelial cells were then sorted by flow cytometry， and Western blot was used to detect the expression of TLR， MyD88， TRAF6， Toll-interleukin receptor domain-containing adaptor inducing interferon-β （TRIF）， inhibitor of κB kinase α （IKKα）， and nuclear factor-κB （NF-κB） in the sorted epithelial cells. Enzyme-linked immunosorbent assay （ELISA） was used to measure the levels of interleukin-1β （IL-1β） and tumor necrosis factor-α （TNF-α） in lung tissue. ResultsAt the transcriptional level， SFJD reversed the expression of TLR signaling pathway genes in respiratory epithelial cells， downregulating multiple TLR signaling pathway-related genes （P<0.01）. At the protein level， SFJD significantly reduced the proportion of respiratory epithelial cells expressing TLR3 （P<0.05）， the expression levels of TLR2， TLR3， TLR4， TRIF， TRAF6， IKKα， and NF-κB in epithelial cells（P<0.05， P<0.01）， as well as the levels of pro-inflammatory cytokines IL-1β and TNF-α in lung tissue （P<0.01）. ConclusionSFJD may alleviate viral pneumonia by suppressing the expression of TLR in respiratory epithelial cells and their subsequent signaling cascades.
