文献类型：期刊文献

英文题名：Galangin Prevents Against Ethanol-Induced Intestinal Barrier Dysfunction and NLRP3 Inflammasome Activation via NF-κB/MAPK Signaling Pathways in Mice and Caco-2 Cells

作者：Zhao, Yanan[1,2,3,4,5];Li, Bin[1,2,3,4,5];Liu, Jiang[1,2,3,4,5];Chen, Lei[1,2,3,4,5];Teng, Hui[1,2,3,4,5]

机构：[1]Guangdong Ocean Univ, Coll Food Sci & Technol, Zhanjiang 524000, Peoples R China;[2]Guangdong Prov Key Lab Aquat Prod Proc & Safety, Zhanjiang 524000, Guangdong, Peoples R China;[3]Guangdong Prov Engn Lab Marine Biol Prod, Zhanjiang 524000, Guangdong, Peoples R China;[4]Guangdong Prov Engn Technol Res Ctr Seafood, Zhanjiang 524000, Guangdong, Peoples R China;[5]Guangdong Higher Educ Inst, Key Lab Adv Proc Aquat Prod, Zhanjiang 524000, Guangdong, Peoples R China

年份：2024

卷号：72

期号：16

起止页码：9376

外文期刊名：JOURNAL OF AGRICULTURAL AND FOOD CHEMISTRY

收录：SCI-EXPANDED(收录号：WOS:001201318000001)、、EI(收录号：20241615920442)、Scopus(收录号：2-s2.0-85190238822)、WOS

基金：This study was supported by the National Natural Science Foundation of China (Grant/Award No. 32372335), the program for Science Research Start-up Foundation of Guangdong Ocean University (No. 060302042312) and Basic and Applied Basic Research Foundation of Guangdong Province (No. 2023A1515110700).

语种：英文

外文关键词：galangin; ethanol; intestinal barrier dysfunction; NF-kappa B; MAPK

外文摘要：The potential of natural phytochemicals in addressing ethanol-related public safety concerns has been garnering attention. Galangin, a potent flavonoid renowned for its antioxidative and anti-inflammatory characteristics, is derived from the galanga plant, and propolis is derived from bees. Here, we documented the effects of galangin on ethanol-stimulated intestinal tight junction damage and investigated its potential protective mechanism in both in vivo and in vitro models, which has not been extensively investigated. Our results revealed that galangin efficaciously mitigated ethanol-induced intestine injury and dysfunction of the intestinal barrier. Concurrently, galangin significantly counteracted the ethanol-induced upregulation of NLRP3 inflammasome-associated proteins and activated the mitogen-activated protein kinase (MAPK) and nuclear factor kappa-B (NF-kappa B) signaling pathways in both the mouse colon and Caco-2 cells. Interestingly, similar to galangin, inhibitors of MAPKs and the NF-kappa B p65 reduced ethanol-induced NLRP3 inflammasome activation and intestinal tight junction damage. To sum up, our results showed that galangin blocks the ethanol-induced perturbation of the intestinal barrier and activation of the NLRP3 inflammasome via the NF-kappa B/MAPK signaling pathways.