Effects of cryptotanshinone on airway inflammation models in asthmatic mice through tweak/fnl4 and tgf-pl/smads signaling pathways
10.3969/j.issn.1001-1978.2019.08.022
- Author:
Chong-Yang WANG
1
Author Information
1. College of Medicine, Yanbian University, Dept of Anatomy
- Publication Type:Journal Article
- Keywords:
Airway inflammation;
Cryptotanshinone;
Cytokine;
Fibroblast growth factor-inducible 14 (fn14);
TNF-related weak inducer of apoptosis (tweak);
Transforming growth factor ß1(tgf-ß1)
- From:
Chinese Pharmacological Bulletin
2019;35(8):1149-1154
- CountryChina
- Language:Chinese
-
Abstract:
Aim To explore the therapeutic effect of cryptotanshinone(CTS) on airway remodeling model of asthmatic mice, and the relationship between its mechanism and the TWEAK/Fn14 and TGF-β1/Smads signaling pathway. Methods Forty female BALB/c mice were used for our study, eight mice as a group, and were assigned into five groups, namely, control group, OVA model group, CTS treatment group (20, 40 mg·kg-1), and Dex positive control group (1 mg·kg-1). HE and PAS staining were used to observe lung histopathological changes in mice; Diff-Quick staining was employed to count the types of cells; ELISA was used to detect the contents of proinflammatory cytokines in BALF; Western blot was applied to analyze the contents of TWEAK, Fn14, TGF-β1, Smad2/3, Smad4 in lung tissues; immunohistochemical method was used to detect the expression levels of TWEAK and TGF-β1 in lung tissues. Results CTS reduced the exudation of inflammatory cells and proliferation of goblet cells; CTS inhibited the generation of EOS, NEU, LYM and the total cells; CTS could reduce the level of proinflammatory cytokines of airway inflammation; the results of Western blot showed that CTS inhibited the protein expression of TWEAK, Fn14, TGF-β1, Smad2/3 and Smad4; immunohistochemical results indicated that CTS increased the expression of TWEAK and TGF-β1 in lung tissues. Conclusions CTS has therapeutic effect on the OVA-induced airway inflammation mouse model through TWEAK/Fn14 and TGF-β1/Smads signaling pathways.