Effect of Viola tianshanica Maxim extract on airway inflammation in asthmatic mice by NLRP3/caspase-1/IL-1β signaling pathway and its mechanism
- VernacularTitle:天山堇菜提取物基于NLRP3/caspase-1/IL-1β信号通路改善哮喘小鼠气道炎症的作用及机制
- Author:
Yu-Zhu SHI
1
;
Yan LIU
;
Lei XU
;
Xue WANG
Author Information
- Keywords: Viola tianshanica Maxim extract; OVA; asthmatic mice; airway inflammation; NLRP3 inflam-masome; mechanism
- From: Chinese Pharmacological Bulletin 2024;40(5):929-936
- CountryChina
- Language:Chinese
- Abstract: Aim To investigate the effect of Viola tianshanica Maxim extract(VTME)on airway inflam-mation in asthmatic mice and the underlying mecha-nism.Methods BALB/c mice were divided into the OVA model group,VTME groups(80,160 and 320 mg·kg-1),Dex group(dexamethasone,80 mg· kg-1)and the control group.OVA and aluminum hy-droxide suspension were adopted to induce asthma models.Mouse alveolar lavage fluid(BALF)was col-lected,then the inflammatory cells in BALF were sor-ted and numbered.The concentrations of TNF-α,IFN-γ and Rantes in BALF,the contents of TNF-α,IFN-γ,IL-17 and MCP-1 in lung,and the concentrations of IgE and Eotaxin in serum were examined by Elisa methods seperately.The pathological changes of lung tissue were inspected by HE staining.The levels of NLRP3 mRNA expression and caspase-1,GSDMD,IL-1 β and NLRP3 protein expression in lung tissue were determined by qRT-PCR and Western blot.Re-sults VTME obviously inhibited the number of total cells and the production of NEU,EOS,LYM,Mon and Bas in BALF.VTME also obviously decreased the levels of TNF-α,IFN-γ and Rantes in BALF,the con-tents of inflammatory factors MCP-1,IFN-γ and IL-17 in lung tissue and the levels of IgE and eotaxin in ser-um.The pathological status of lung tissue was obvious-ly improved.In lung tissue,the level of NLRP3 mR-NA expression obviously declined,and the contents of NLRP3,caspase-1,GSDMD and IL-1 β protein expres-sion were also obviously reduced.Conclusions VT-ME has a notable protective effect on asthmatic mice,and its mechanism is likely due to the restriction of NL-RP3/caspase-1/IL-1 β signaling pathway.
