Jiebiao Qingli Decoction Regulates TLR7/MAPK/NF-κB Pathway to Prevent and Treat Pneumonia Induced by IAV Infection
10.13422/j.cnki.syfjx.20250409
- VernacularTitle:解表清里方通过调控TLR7/MAPK/NF-κB通路对甲流病毒感染所致肺炎的防治作用
- Author:
Yu MING
1
;
Yichuan MA
2
;
Ruiqi YAO
3
;
Yan CHAO
4
;
Hongchun ZHANG
5
Author Information
1. Institute of Basic Research in Clinical Medicine，China Academy of Chinese Medical Sciences， Beijing 100700，China
2. Shenzhen Bao'an Authentic Traditional Chinese Medicine Therapy Hospital，Shenzhen 518101，China
3. Shenzhen Nanshan District Hospital of Traditional Chinese Medicine，Shenzhen 518000，China
4. Beijing Oriental Yunjia Pharmaceuticals Co. Ltd.，Beijing 100029，China
5. Clinical Research Center for Respiratory Diseases，China-Japan Friendship Hospital，Beijing 100029，China
- Publication Type:Journal Article
- Keywords:
Jiebiao Qingli decoction;
influenza A virus （IAV）;
influenza;
Toll-like receptor 7 （TLR7）/mitogen-activated protein kinase （MAPK）/nuclear factor-kappa B （NF-κB） signaling pathway;
cytokines
- From:
Chinese Journal of Experimental Traditional Medical Formulae
2025;31(11):173-181
- CountryChina
- Language:Chinese
-
Abstract:
ObjectiveTo explore the mechanism of Jiebiao Qingli decoction （JQD） in treating pneumonia caused by influenza A virus （IAV） infection. MethodsA total of 132 Balb/c mice were randomly assigned into normal control （NC）， model control （IAV）， oseltamivir （OSV， 37.5 mg·kg-1）， and high-， medium-， low-dose JQD （H-， M-， and L-JQD： 6.05， 3.02， and 1.51 g·kg-1， respectively） groups. The NC group was treated with normal saline nasal drops， and the other groups were intranasally inoculated with A/Brisbane/02/2018 （H1N1） ［pdm09-like virus （H1N1）］ for the modeling of IAV infection. Two hours post-modeling， the NC and IAV groups were administrated with normal saline by gavage， while other groups received corresponding drugs for 7 d. The body mass， survival status， and deaths of mice were recorded daily during the administration of the drugs. On days 3 and 7， the lung index was measured for mice in each group. Pathological changes in the lung tissue were observed via hematoxylin-eosin staining. Real-time fluorescence quantitative polymerase chain reaction （Real-time PCR） was conducted to measure the viral load （IAV-M） and the mRNA levels of Toll-like receptor 7 （TLR7）， p38 mitogen-activated protein kinase （p38 MAPK）， and nuclear factor-kappa B （NF-κB） in the lung tissue. Western blot was employed to measure the protein levels of p38 MAPK and NF-κB. Enzyme-linked immunosorbent assay was used to quantify serum levels of interleukin-2 （IL-2）， interleukin-6 （IL-6）， and tumor necrosis factor-alpha （TNF-α）. ResultsCompared with the NC group， the IAV group showed reduced survival quality and survival days （P<0.01）， lung congestion， inflammatory cell infiltration， elevated lung index （P<0.01）， increased viral load （P<0.01）， upregulated TLR7， p38 MAPK， and NF-κB levels （P<0.05， P<0.01）， decreased IL-2 level （P<0.01）， and elevated IL-6 and TNF-α levels （P<0.01）. Compared with the IAV group， H-JQD prolonged survival days （P<0.05）. All JQD groups alleviated pathological changes in the lung tissue and reduced the lung index （P<0.01）. M-JQD and H-JQD decreased the viral load （P<0.01）. H-JQD downregulated the mRNA levels of TLR7， p38 MAPK， and NF-κB （P<0.05， P<0.01） and the protein levels of p38 MAPK and NF-κB （P<0.01）， increased the serum IL-2 level （P<0.01）， and lowered the IL-6 and TNF-α levels （P<0.05， P<0.01）. M-JQD downregulated the mRNA level of NF-κB （P<0.01） and the protein level of p38 MAPK （P<0.05）， elevated the IL-2 level （P<0.01）， and lowered the TNF-α level （P<0.01）. ConclusionM- and H-JQD can prevent and control IAV infection-induced pneumonia dose-dependently by inhibiting the TLR7/MAPK/NF-κB signaling pathway， increasing IL-2， and reducing excessive secretion of IL-6 and TNF-α.
