Capsaicin (CAP) exerts a protective effect against ethanol-induced oxidative gastric mucosal injury by modulating the chemokine receptor 4 (CCR4)/Src/p47phox signaling pathway both in vitro and in vivo.
10.1016/S1875-5364(25)60823-5
- Author:
Zhiru YANG
1
;
Haolin GUO
2
;
Pengfei ZHANG
3
;
Kairui LIU
1
;
Junli BA
1
;
Xue BAI
1
;
Shiti SHAMA
1
;
Bo ZHANG
4
;
Xiaoning GAO
5
;
Jun KANG
6
Author Information
1. School of Life Sciences, Tianjin University, Tianjin 300072, China.
2. School of Traditional Chinese Medicine, Beijing University of Chinese Medicine, Beijing 102499, China.
3. Tianjin Pharmaceutical and Cosmetic Evaluation and Inspection Center, Tianjin 300191, China.
4. Institute for TCM-X, MOE Key Laboratory of Bioinformatics, Bioinformatics Division, BNRist, Department of Automation, Tsinghua University, Beijing 100084, China; Institute of Biomedical Research, Henan Academy of Sciences, Zhengzhou 450046, China. Electronic address: zhangbo.2007@tsinghua.org.cn.
5. School of Life Sciences, Tianjin University, Tianjin 300072, China. Electronic address: xiaoninggao@tju.edu.cn.
6. School of Life Sciences, Tianjin University, Tianjin 300072, China. Electronic address: jun.kang@tju.edu.cn.
- Publication Type:Journal Article
- Keywords:
Capsaicin;
Chemokine signaling;
Gastric mucosal damage;
NF-κB p65
- MeSH:
Ethanol/toxicity*;
Animals;
Gastric Mucosa/metabolism*;
Signal Transduction/drug effects*;
Oxidative Stress/drug effects*;
Capsaicin/pharmacology*;
Male;
NADPH Oxidases/genetics*;
Mice;
Humans;
src-Family Kinases/genetics*
- From:
Chinese Journal of Natural Medicines (English Ed.)
2025;23(2):191-202
- CountryChina
- Language:English
-
Abstract:
Ethanol (EtOH) is a common trigger for gastric mucosal diseases, and mitigating oxidative stress is essential for attenuating gastric mucosal damage. Capsaicin (CAP) has been identified as a potential agent to counteract oxidative damage in the gastric mucosa; however, its precise mechanism remains unclear. This study demonstrates that CAP alleviates EtOH-induced gastric mucosal injuries through two primary pathways: by suppressing the chemokine receptor 4 (CCR4)/Src/p47phox axis, thereby reducing oxidative stress, and by inhibiting the phosphorylation and nuclear translocation of nuclear factor-κB p65 (NF-κB) p65, resulting in diminished inflammatory responses. These findings elucidate the mechanistic pathways of CAP and provide a theoretical foundation for its potential therapeutic application in the treatment of gastric mucosal injuries.
