菊粉
溃疡性结肠炎
党参
代谢组学
果聚糖
传统医学
医学
化学
食品科学
色谱法
中医药
疾病
内科学
蔗糖
病理
替代医学
作者
Jiangtao Zhou,J Wang,D G Li,Zhenyu Zhang,Changjian Wang,Xuepeng Zhang,Xide Xu,Jianping Gao
出处
期刊:American Journal of Physiology-gastrointestinal and Liver Physiology
[American Physiological Society]
日期:2024-01-09
标识
DOI:10.1152/ajpgi.00214.2023
摘要
Ulcerative colitis (UC) is an inflammatory disease with abdominal pain, diarrhea and bloody stool as the main symptoms. Several studies have confirmed that polysaccharides are effective against UC. It is commonly accepted that the traditional benefits of Radix Codonopsis can be attributed to its polysaccharide contents, and inulin-type fructan CP-A is the main active monomer in the polysaccharide components. Herein, we established a 2, 4, 6-trinitrobenzene sulfonic acid (TNBS)-induced UC rat model and lipopolysaccharide (LPS)-induced colonic epithelial cell model (NCM460) to investigate the effect of CP-A on UC. Untargeted metabolomics studies were conducted to identify differential metabolites using ultra-high performance liquid chromatography quadrupole time-of-flight tandem mass spectrometry (UHPLC-Q-TOF/MS) and enrich metabolic pathways in rat serum. The in vivo assays demonstrated that CP-A reduces colonic macroscopic injury, disease activity index (DAI), histopathological score, interleukin (IL)-8 and tumor necrosis factor-alpha (TNF-α) levels, as well as the expression of intercellular adhesion molecules. On the other hand, increase the IL-10 and transforming growth factor- beta (TGF-β) levels. The in vitro experiments indicated that CP-A treatment could reduce nitric oxide (NO) and IL-1β after LPS stimulation. The metabolomics results suggested that CP-A therapy for UC may be related to the mTOR signaling pathway. The in vitro and in vivo validation of the pathway showed similar results, indicating that CP-A alleviates UC by preventing the activation of mTOR/p70S6K signaling pathway. These findings offer a fresh approach to treating UC and a theoretical foundation for the future advancement of CP-A.
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