Staphylea bumalda Alleviates Dextran Sulfate Sodium-Induced Ulcerative Colitis in Mice by Regulating Inflammatory Cytokines, Oxidative Stress, and Maintaining Gut Homeostasis

被引:0
|
作者
Wang, Lu [1 ]
Long, Sha [1 ]
Zeng, Qi [1 ]
Dong, Wanrong [1 ]
Li, Yaoyao [1 ]
Su, Jiangtao [1 ]
Chen, Yuxin [1 ,2 ]
Zhou, Gao [1 ,2 ,3 ]
机构
[1] Minist Educ & Hubei Prov, Minist Educ, Cooperat Innovat Ctr Ind Fermentat, Hubei Key Lab Ind Microbiol,Key Lab Fermentat Engn, Wuhan 430068, Peoples R China
[2] Hubei Univ Technol, Natl Ctr Cellular Regulat & Mol Pharmaceut 111, Sch Life & Hlth Sci, Wuhan 430068, Peoples R China
[3] Postdoctoral Res Ctr Mayinglong Pharmaceut Grp Co, Wuhan 430064, Peoples R China
来源
MOLECULES | 2024年 / 29卷 / 21期
基金
中国国家自然科学基金;
关键词
<italic>Staphylea bumalda</italic>; ulcerative colitis; inflammatory factor; oxidative stress; gut flora homeostasis; LIQUID-CHROMATOGRAPHY; PHENOLIC-COMPOUNDS; IN-VITRO; LC-MS/MS; IDENTIFICATION; COMPONENTS; EXTRACT;
D O I
10.3390/molecules29215030
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Staphylea bumalda is a rare medicine and edible shrub native to the temperate regions of Asia, possessing significant medicinal potential. In this study, the components of S. bumalda tender leaves and buds extract (SBE) were analyzed and identified by HPLC and LC/MS method, and the safety of SBE was evaluated through mouse acute toxicity models. The protective effects of SBE on dextran sulfate sodium (DSS)-induced ulcerative colitis (UC) in mice were investigated in terms of inflammatory factor levels, oxidative stress, and gut microorganisms. Results showed that hyperoside, kaempferol-3-O-rutinoside, isorhoifolin, and rutin were the main components of the extract, and SBE demonstrated good safety in experimental mice. SBE could alleviate weight losing, disease activity index (DAI) raising, and colon shortening in mice. Pathological section results showed that the inflammatory cell infiltration decreased significantly, and the number of goblet cells increased significantly in the SBE group. After SBE treatment, interleukin-6 (IL-6), interleukin-1 beta (IL-1 beta), and tumor necrosis factor-alpha (TNF-alpha) levels in serum were significantly decreased, and the levels of myeloperoxidase (MPO) and nitric oxide (NO) in colon tissues were significantly decreased. SBE inhibited gut inflammation by increasing Lactobacillus. In summary, SBE played a therapeutic role in UC mice by relieving colon injury, reducing inflammatory factor levels, and maintaining gut flora homeostasis. SBE is expected to become an auxiliary means to participate in the prevention and treatment of UC.
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页数:18
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