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丁酸通过抑制JAK2/STAT3/SOCS1信号通路增强EHLJ7对溃疡性结肠炎的治疗作用。

Butyric Acid Increases the Therapeutic Effect of EHLJ7 on Ulcerative Colitis by Inhibiting JAK2/STAT3/SOCS1 Signaling Pathway.

作者信息

Tang Xiaonan, Li Xiang, Wang Yufei, Zhang ZhiHui, Deng AnJun, Wang WenJie, Zhang Haijing, Qin Hailin, Wu LianQiu

机构信息

Laboratory of Bioactive Substances and Functions of Natural Medicines, Institute of Materia Medica, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China.

出版信息

Front Pharmacol. 2020 Jan 22;10:1553. doi: 10.3389/fphar.2019.01553. eCollection 2019.

DOI:10.3389/fphar.2019.01553
PMID:32038241
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6987075/
Abstract

Ulcerative colitis (UC) is a refractory chronic disease characterized by bloody diarrhea and mucosal or submucosal ulcers. There is an urgent need of new drugs for the treatment of ulcerative colitis. EHLJ7 is a quaternary coptisine derivative. Herein, we explored the therapeutic effect of EHLJ7 on dextran sodium sulfate (DSS)-induced ulcerative colitis (UC) in mice. Results showed that EHLJ7 have good effects on DSS-induced colitis. EHLJ7 significantly improved symptoms induced by DSS including of weight loss, colon contracture, disease activity index (DAI), inflammatory infiltration, and so on. Furthermore, results showed that EHLJ7 could enhance short-chain fatty acids (SCFAs) production especially butyric acid, suggesting that EHLJ7 could improve the metabolic disorder of intestinal flora to a certain extent. Further study indicated that EHLJ7 could cooperate with butyrate to exert its anti-ulcerative colitis effect by inhibiting the activation of janus kinase 2 (JAK2)/signal transducer and activator of transcription 3 (STAT3)/suppressor of cytokine signaling 1 (SOCS1) pathway. Therefore, EHLJ7 has a potential to be developed as a candidate for the treatment of colitis.

摘要

溃疡性结肠炎（UC）是一种难治性慢性病，其特征为血性腹泻以及黏膜或黏膜下溃疡。治疗溃疡性结肠炎急需新型药物。EHLJ7是一种季铵型黄连碱衍生物。在此，我们探究了EHLJ7对葡聚糖硫酸钠（DSS）诱导的小鼠溃疡性结肠炎（UC）的治疗效果。结果显示，EHLJ7对DSS诱导的结肠炎有良好效果。EHLJ7显著改善了DSS诱导的症状，包括体重减轻、结肠挛缩、疾病活动指数（DAI）、炎症浸润等。此外，结果表明EHLJ7可增强短链脂肪酸（SCFAs）的产生，尤其是丁酸，这表明EHLJ7可在一定程度上改善肠道菌群的代谢紊乱。进一步研究表明，EHLJ7可与丁酸盐协同作用，通过抑制 janus激酶2（JAK2）/信号转导子和转录激活子3（STAT3）/细胞因子信号传导抑制因子1（SOCS1）通路的激活来发挥其抗溃疡性结肠炎的作用。因此，EHLJ7有潜力被开发成为治疗结肠炎的候选药物。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e20b/6987075/2128496c7727/fphar-10-01553-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e20b/6987075/6659855c490f/fphar-10-01553-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e20b/6987075/528bf46a76ba/fphar-10-01553-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e20b/6987075/74f6f748f6ef/fphar-10-01553-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e20b/6987075/fbfa6bfe0a07/fphar-10-01553-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e20b/6987075/045cb7d4da07/fphar-10-01553-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e20b/6987075/2128496c7727/fphar-10-01553-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e20b/6987075/6659855c490f/fphar-10-01553-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e20b/6987075/528bf46a76ba/fphar-10-01553-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e20b/6987075/74f6f748f6ef/fphar-10-01553-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e20b/6987075/fbfa6bfe0a07/fphar-10-01553-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e20b/6987075/045cb7d4da07/fphar-10-01553-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e20b/6987075/2128496c7727/fphar-10-01553-g006.jpg

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