Shaoyao Decoction Inhibits Inflammation and Improves Intestinal Barrier Function in Mice With Dextran Sulfate Sodium-Induced Colitis

被引:22
|
作者
Chi, Honggang [1 ,2 ]
Wang, Dan [3 ]
Chen, Mengting [3 ]
Lin, Jiantao [3 ]
Zhang, Shuhua [1 ]
Yu, Fengyan [4 ]
Zhou, Jun [5 ]
Zheng, Xuebao [6 ]
Zou, Ying [1 ,7 ]
机构
[1] Guangdong Med Univ, Dept Tradit Chinese Med, Clin Med Coll 2, Dongguan, Peoples R China
[2] Guangdong Med Univ, Dept Tradit Chinese Med, Dongguan Affiliated Hosp 1, Dongguan, Peoples R China
[3] Guangdong Med Univ, Dept Pharmacol, Dongguan, Peoples R China
[4] Guangdong Med Univ, Clin Med Coll 2, Dongguan, Peoples R China
[5] Southern Med Univ, Nanfang Hosp, Dept Pathol, Guangzhou, Peoples R China
[6] Guangzhou Univ Chinese Med, Acad Chinese Med, Math Engn, Guangzhou, Peoples R China
[7] Dongguan Liaobu Hosp, Dept Tradit Chinese Med, Dongguan, Peoples R China
基金
中国国家自然科学基金;
关键词
inflammatory bowel disease; colitis; intestinal barrier function; shaoyao decoction; traditional Chinese medicine; mucus barrier; epithelial barrier; NF-KAPPA-B; BOWEL-DISEASE; COLORECTAL TUMORIGENESIS; ULCERATIVE-COLITIS; SIGNAL TRANSDUCERS; CYTOKINES; MACROPHAGES; HOMEOSTASIS; DISRUPTION; ACTIVATION;
D O I
10.3389/fphar.2021.524287
中图分类号
R9 [药学];
学科分类号
1007 ;
摘要
Shaoyao decoction (SYD), a classical traditional Chinese medicine formula, is effective for the treatment of inflammatory bowel disease (IBD). This study was designed to investigate the therapeutic effects of SYD on IBD and possible mechanisms. Dextran sulfate sodium (DSS, 3.5%) was used to induce colitis in C57BL/6 mice. Disease phenotypes were investigated based on disease activity index (DAI), colon length, and microscopic and macroscopic scores. Additionally, the presence of proinflammatory cytokines, immune cell infiltrates, intestinal cell proliferation, apoptosis, epithelial permeability, signal transducer and activator of transcription 3 (STAT3), and nuclear factor-kappa B (NF-kappa B) signaling, as well as the intestinal mucosal barrier function, were investigated. The administration of SYD significantly ameliorated the clinical signs, suppressed the levels of proinflammatory cytokines, and reduced immune cell infiltrates into colonic tissues of DSS-induced colitis model mice. SYD also significantly reduced the DSS-induced activation of STAT3 and NF-kappa B signaling. Furthermore, SYD promoted epithelial integrity by regulating epithelial cell apoptosis and epithelial permeability. Finally, we demonstrated that SYD protected the intestinal barrier function by significantly regulating the mucus layer genes Muc1, Muc2, Muc4, and Tff3, as well as the epithelial barrier genes Z O -1 and Occludin. Our results indicate that SYD has a protective effect on DSS-induced colitis, which is attributable to its anti-inflammatory activity and intestinal barrier function-enhancing effects. These results provide valuable insights into the pharmacological actions of SYD for the treatment of IBD.
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页数:11
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