Evodiamine prevents dextran sulfate sodium-induced murine experimental colitis via the regulation of NF-κB and NLRP3 inflammasome

Biomedicine & Pharmacotherapy

Kunpeng Zhu¹  Yunhe Fu²  Hongyang Cao²  Naisheng Zhang²  Jiuxi Liu²  Peng Shen²  Zecai Zhang²  Xiaojie Lu²  Yanxin Li²  Xin Yuan²  Yongguo Cao²  Yue Jing² 

[1] Key laboratory for Zoonosis, Ministry of Education, Changchun, 130062, People’s Republic of China;College of Veterinary Medicine, Jilin University, Changchun, 130062, People’s Republic of China;

关键词: Evodiamine;    Colitis;    Inflammation;    Intestinal microbiota;    Intestinal barrier;   

DOI  :  

来源: DOAJ

【 摘 要 】

Evodiamine (EVO), an extraction from the traditional Chinese medicine Evodia rutaecarpa, has been reported to possess anti-inflammatory, anti-tumor and other pharmacological activities. However, the effectiveness of EVO to relieve dextran sodium sulfate (DSS)-induced ulcerative colitis (UC) has not been evaluated. In this study, the protective effects and mechanisms of EVO on DSS-induced UC mice were investigated. The results indicated that treatment with EVO ameliorated DSS-induced UC mice body weight loss, disease activity index (DAI), colon length shortening, colonic pathological damage, and myeloperoxidase (MPO) activity. The production of TNF-α, IL-1β and IL-6 was also significantly inhibited by EVO. Further mechanistic results showed that EVO restrained the inflammation by regulating NF-κB signal and NLRP3 inflammasome. Furthermore, results also showed that EVO contributed to the tight junction (TJ) architecture integrity by modulating the expression of zonula occludens-1 (ZO-1) and occludin during colitis. Surprisingly, treatment with EVO reduced the concentration of plasmatic lipopolysaccharide (LPS) and re-balanced the levels of Escherichia coli and Lactobacillus. These findings suggested that EVO may have a potential protective effect on DSS-induced colitis and may be useful for the prevention and treatment of UC.

【 授权许可】

Unknown