Kui Jie Tong Ameliorates Ulcerative Colitis by Regulating Gut Microbiota and NLRP3/Caspase-1 Classical Pyroptosis Signaling Pathway
Autor: | Shigui Xue, Yan Xue, Danbo Dou, Huan Wu, Ping Zhang, Yang Gao, Yini Tang, Zehua Xia, Sen Yang, Sizhen Gu |
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Jazyk: | angličtina |
Rok vydání: | 2022 |
Předmět: |
Article Subject
Colon Caspase 1 Biochemistry (medical) Clinical Biochemistry Interleukin-18 General Medicine Interleukin-33 Gastrointestinal Microbiome Rats Rats Sprague-Dawley Disease Models Animal Tandem Mass Spectrometry RNA Ribosomal 16S NLR Family Pyrin Domain-Containing 3 Protein Pyroptosis Genetics Animals Colitis Ulcerative Molecular Biology Chromatography Liquid Signal Transduction |
Zdroj: | Disease Markers. |
ISSN: | 0278-0240 |
DOI: | 10.1155/2022/2782112 |
Popis: | Ulcerative colitis (UC) is one of the most refractory digestive diseases in the world. Kui jie tong (KJT) is an effective traditional Chinese medicine used clinically to treat UC. This study observed the regulatory effects of KJT on NIMA-related kinase 7- (NEK7-) activated nod-like receptor protein-3 (NLRP3)/caspase-1 classical pyroptosis pathway and intestinal flora in UC model rats. KJT components were analyzed using an ultraperformance liquid chromatography-tandem mass spectrometer (UPLC-MS/MS). A UC Sprague Dawley (SD) rat model was established using sodium dextran sulfate (DSS). Rats were randomly divided into four groups: control group (CG), UC model group (UG), KJT group (KG), and sulfasalazine (SASP) group (SG). After seven days of intervention, each group’s body weight, disease activity index (DAI) scores, and colon length were recorded. Intestinal mucosal injury to each group was observed using hematoxylin-eosin staining. Additionally, we investigated the expression levels of NEK7, NLRP3, ASC, caspase-1, and GSDMD in intestinal mucosa, as well as serum interleukin- (IL-) 1β, IL-18, and IL-33 proinflammatory factors. Intestinal microflora was analyzed using 16s rRNA sequencing. KJT controlled weight loss; decreased DAI scores; restored colon length; improved pathological injury in the colon; inhibited NEK7, NLRP3, ASC, caspase-1, cleaved-caspase-1, GSDMD, and GSDMD-N expression; and decreased IL-1β, IL-18, and IL-33 contents in UG rats’ serum and colon tissue (P |
Databáze: | OpenAIRE |
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