文献类型：期刊文献

英文题名：TXM-CB13 Improves the Intestinal Mucosal Barrier and Alleviates Colitis by Inhibiting the ROS/TXNIP/TRX/NLRP3 and TLR4/MyD88/NF-κB/NLRP3 Pathways

作者：Cao, Ruijie[1];Zhou, Jinhui[1];Liu, Jiale[1];Wang, Yaxuan[1];Dai, Yandong[1];Jiang, Yun[1];Yamauchi, Akira[2];Atlas, Daphne[3];Jin, Tiancheng[1];Zhou, Jiedong[1];Wang, Cuixue[1];Tan, Qihuan[1];Chen, Yifei[1];Yodoi, Junji[4];Tian, Hai[1,5]

机构：[1]Shaoxing Univ, Med Coll, Dept Basic Med, Shaoxing, Peoples R China;[2]Misugi Kai Sato Hosp Breast Ctr, Dept Breast Surg, Hirakata, Osaka, Japan;[3]Hebrew Univ Jerusalem, Inst Life Sci, Dept Biol Chem, IL-91904 Jerusalem, Israel;[4]Kyoto Univ, Inst Virus Res, Dept Biol Response, Lab Infect & Prevent, Kyoto, Japan;[5]Jiaozhimei Biotechnol Shaoxing Co Ltd, Shaoxing, Peoples R China

年份：2025

外文期刊名：INFLAMMATION

收录：SCI-EXPANDED(收录号：WOS:001444627200001)、、WOS

语种：英文

外文关键词：TXM-CB13; Inflammatory bowel disease; NLRP3; TXNIP; NF-kappa B

外文摘要：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-1 beta 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-kappa B pathways, including p-I kappa B-alpha/I kappa B-alpha and p-NF-kappa B-p65/NF-kappa B-p65. This inhibition further reduced the activation of the NLRP3 inflammasome components, NLRP3, ASC, Caspase-1, GSDMD, and IL-1 beta. 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-kappa B/NLRP3 and ROS/TXNIP/TRX/NLRP3 pathways.