Deoxyschizandrin treats mice with ulcerative colitis possibly via the TLR4/NF-κB signaling pathway

被引:6
|
作者
Yu, Sheng [1 ]
Qian, Haihua [2 ]
机构
[1] Nanjing Univ Tradit Chinese Med, Surg Tradit Chinese Med, Clin Med Coll 1, Nanjing 210000, Jiangsu, Peoples R China
[2] North Hosp Jiangsu Prov Tradit Chinese Med, Dept Anorectal Dis, 155 Hanzhong Rd, Nanjing 210000, Jiangsu, Peoples R China
来源
关键词
Deoxyschizandrin; ulcerative colitis; TLR4/NF-kappa B; mice; IN-VITRO; INFLAMMATION; SCHISANDRA; EXTRACTS; PLASMA; CANCER; INJURY;
D O I
暂无
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Objective: This study aimed to investigate the effects and mechanisms of deoxyschizandrin (DSD) on treatment of ulcerative colitis (UC). Methods: The models of mice with UC were established through dextran sulfate sodium (DSS) administration, and the successful models were treated with DSD. The therapeutic effects of DSD on UC mice were evaluated and its behind mechanisms were analyzed. Results: After DSS induction, the mice showed increased body weight and colon length, worse disease activity index (DAI) and body inflammation, oxidative stress injury and increased apoptosis of colonic epithelial cells, which were remarkably relieved after DSD intervention. Besides, the levels of TLR4, MyD88 and NF-kappa B in the colon tissues were elevated in UC mouse models, while DSD treatment reduced the levels of these markers. Conclusion: DSD can alleviate the symptoms of mice with DSS-induced UC via inhibiting body inflammation, improving oxidative stress and reducing the apoptosis of colonic epithelial cells, which may be attributed to DSD inhibition of the TLR4/NF-kappa B signaling pathway.
引用
收藏
页码:3856 / 3863
页数:8
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