ArticleInflammation2025
TXM-CB13 Improves the Intestinal Mucosal Barrier and Alleviates Colitis by Inhibiting the ROS/TXNIP/TRX/NLRP3 and TLR4/MyD88/NF-κB/NLRP3 Pathways.
Article in Inflammation, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- Identification MYD88 as a candidate molecule of sodium overload-induced cell death in myocardial ischemia-reperfusion injury.Journal of cardiothoracic surgery · 2026Article
- Effects of Compound Yeast Culture and Yeast Cell Wall Polysaccharide on Intestinal Barrier Function in Mongolian Ram Lambs.Animals : an open access journal from MDPI · 2026Article
- Mechanisms and therapeutic prospects of DNA methylation-mucosal innate immunity crosstalk in inflammatory bowel disease.Frontiers in immunology · 2026Review
- Acupuncture modulates the microbiota-gut-brain axis to treat irritable bowel syndrome: a mechanistic exploration.Frontiers in neuroscience · 2026Review
- Lycopene Antagonizes Deoxynivalenol-Induced Porcine Intestinal Epithelial Cell Senescence by Inhibiting TXNIP-Mediated NLRP3 Inflammasome Activation.Research (Washington, D.C.) · 2026Article
- Targeting neurodegeneration and inflammation with thioredoxin-mimetic peptides.Redox biology · 2025Review
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15 authors.
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Abstract
The activation of inflammasomes (NLRP3 and NLRP1) is central to the pathogenesis of inflammatory bowel disease (IBD). Here we examined the protective effects of a thioredoxin-mimetic peptide CB13 (TXM-CB13), known for its antioxidative stress and anti-inflammatory properties. We examined the effects of TXM-CB13 on dextran sulfate sodium (DSS)-induced colitis and lipopolysaccharide (LPS)-induced NLRP3 inflammasome activation in RAW264.7 macrophages. TXM-CB13 appeared to alleviate symptoms of DSS-induced colitis and to significantly suppress the protein and mRNA levels of NLRP3, Mlck, and IL-1β in colonic tissues. Additionally, TXM-CB13 treatment increased the levels of the intestinal barrier proteins Occludin, ZO-1, and NLRP1, as shown through immunohistochemistry and Western blot analysis. In vitro, TXM-CB13 inhibited LPS-induced TLR4 signaling, reducing MyD88 levels and consequently attenuating the activation of the NF-κB pathways, including p-IκB-α/IκB-α and p-NF-κB-p65/NF-κB-p65. This inhibition further reduced the activation of the NLRP3 inflammasome components, NLRP3, ASC, Caspase-1, GSDMD, and IL-1β. In addition, TXM-CB13 prevented the ROS-mediated dissociation of TXNIP from TRX, inhibiting NLRP3 activation. These findings suggest that TXM-CB13 is a potential therapeutic candidate for IBD through its modulation of the TLR4/MyD88/NF-κB/NLRP3 and ROS/TXNIP/TRX/NLRP3 pathways.
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