A new phenolic acid isolated from Salvia miltiorrhiza ameliorates OVA-induced allergic asthma by regulation of Th17/Treg cells and inflammation through the TLR4 pathway.
10.1016/j.cjnm.2025.100007
- Author:
Zeng MENGNAN
1
;
Wu YUANYUAN
2
;
Ren YINGJIE
2
;
Jiao XIANMIAN
2
;
Chang FANGZHUO
2
;
Wang YUANYUAN
2
;
Feng WEISHENG
3
;
Zheng XIAOKE
4
,
5
Author Information
1. College of Pharmacy, Henan University of Chinese Medicine, Zhengzhou 450000, China; The Engineering and Technology Center for Chinese Medicine Development of Henan Province, Zhengzhou 450000, China; Co-construction of Collaborative Innovation Center for Chinese Medicine and Respiratory Diseases by Henan&Education Ministry of China, Zhengzhou 450000, China.
2. College of Pharmacy, Henan University of Chinese Medicine, Zhengzhou 450000, China; The Engineering and Technology Center for Chinese Medicine Development of Henan Province, Zhengzhou 450000, China.
3. College of Pharmacy, Henan University of Chinese Medicine, Zhengzhou 450000, China; The Engineering and Technology Center for Chinese Medicine Development of Henan Province, Zhengzhou 450000, China; Co-construction of Collaborative Innovation Center for Chinese Medicine and Respiratory Diseases by Henan&Education Ministry of China, Zhengzhou 450000, China. Electronic address: fwsh@hactcm.edu.cn.
4. College of Pharmacy, Henan University of Chinese Medicine, Zhengzhou 450000, China; The Engineering and Technology Center for Chinese Medicine Development of Henan Province, Zhengzhou 450000, China; Co-construction of Collaborative Innovation Center for Chinese Medicine and Respiratory Diseases by Henan&Education Ministry of China, Zhengzhou 450000, China. Electronic address: zhengxk.2006@
5. com.
- Publication Type:Journal Article
- Keywords:
Asthma;
Co-culture;
Phenolic acid;
Salvia miltiorrhiza;
TLR4
- From:
Chinese Journal of Natural Medicines (English Ed.)
2025;23(12):100007-100007
- CountryChina
- Language:English
-
Abstract:
Salvia miltiorrhiza (S. miltiorrhiza) represents a crucial component of traditional Chinese medicine, demonstrating effects on blood circulation activation and stasis removal, and has been widely utilized in asthma treatment. This study isolated a novel phenolic acid (S1) from S. miltiorrhiza and investigated its anti-asthmatic activity and underlying mechanisms for the first time. An allergic asthma (AA) model was established using ovalbumin (OVA). The mechanism of S1's effects on AA was investigated using multi-factor joint analysis, flow cytometry, and co-culture systems to facilitate clinical asthma treatment. S1 (10 or 20 mg·kg-1) was administered daily to mice with OVA-induced AA (OVA-AA) during days 21-25. The study examined airway responsiveness, lung damage, inflammation, and levels of immunoglobulin E (IgE), PGD2, interleukins (IL-4, 5, 10, 13, 17A), tumor necrosis factor α (TNF-α), GM-CSF, CXCL1, CCL11, and mMCP-1. Additionally, mast cell (MC) activation and degranulation were explored, along with T helper type 17 (Th17)/Treg immune cells and TLR4 pathway biomarkers. The antagonistic activity of that specific antagonist of TLR4 (TAK-242) (1 µmol·L-1), a specific TLR4 blocker, against S1 (10 µmol·L-1) was examined in co-cultured 16HBE cells and bone marrow-derived cells (BMDCs) or splenic lymphocytes (SLs) induced with LPS (1 µg·mL-1) to elucidate the TLR4 pathway's mediating role. S1 demonstrated reduced airway responsiveness, lung damage, and inflammation, with downregulation of IgE, PGD2, interleukins, TNF-α, GM-CSF, CXCL1, CCL11, and mMCP-1. It also impeded MC activation and degranulation, upregulated IL-10, and influenced Th17/Treg immune cell transformation following OVA challenge. Furthermore, S1 inhibited the TLR4 pathway in OVA-AA mice, and TLR4 antagonism enhanced S1's positive effects. Analysis using an OVA-AA mouse model demonstrated that S1 alleviates AA clinical symptoms, restores lung function, and inhibits airway response. S1's therapeutic effects occur through regulation of Th17/Treg immune cells and inflammation, attributable at least partially to the TLR4 pathway. This study provides molecular justification for S1 in AA treatment.
