文献类型：期刊文献

英文题名：Butyrolactone-I from marine fungi alleviates intestinal barrier damage caused by DSS through regulating lactobacillus johnsonii and its metabolites in the intestine of mice

作者：Chen, Shengwei[1,2];Niu, Xueting[1,2];Zhang, Yi[3];Wen, Jiaying[1,2];Bao, Minglong[1,2];Li, Yin[1,2];Gao, Yuan[1,2];Wang, Xinchen[1,2];Liu, Xiaoxi[1];Yong, Yanhong[1];Yu, Zhichao[1];Ma, Xingbing[1];Eun, Jong-Bang[4];Shim, Jae-Han[5];Abd El-Aty, A. M.[6,7];Ju, Xianghong[1,2]

机构：[1]Guangdong Ocean Univ, Coll Coastal Agr Sci, 1 Haida Rd, Zhanjiang 524088, Guangdong, Peoples R China;[2]Guangdong Ocean Univ, Shenzheng Inst, Org X, Shenzheng, Peoples R China;[3]Guangdong Ocean Univ, Coll Food Sci & Technol, Zhanjiang, Peoples R China;[4]Chonnam Natl Univ, Dept Food Sci & Technol, Gwangju, South Korea;[5]Chonnam Natl Univ, Biotechnol Res Inst, Nat Prod Chem Lab, Gwangju, South Korea;[6]Cairo Univ, Fac Vet Med, Dept Pharmacol, Giza, Egypt;[7]Ataturk Univ, Med Fac, Dept Med Pharmacol, Erzurum, Turkiye

年份：2025

卷号：135

外文期刊名：JOURNAL OF NUTRITIONAL BIOCHEMISTRY

收录：SCI-EXPANDED(收录号：WOS:001359241600001)、、Scopus(收录号：2-s2.0-85209092308)、WOS

基金：This study was supported by the National Natural Science Foundation of China [grant numbers: 32273077] ; The Innovation Team Project of Guangdong Provincial Department of Education [grant number: 2022KCXTD014] ; Guangdong Postgraduate Education Innovation Project [grant number: 040510052201] ; the Project of Enhancing School with Innovation of Guangdong Ocean University [grant number: GDOU230419057] and the Program for Scientific Research Start-Fund of Guangdong Ocean University [grant number: 101402/R17088] ; the Basic Research Project of Shenzhen Science and Technology Innovation Commission [JCYJ20220530162008018] .

语种：英文

外文关键词：Butyrolactone-I; DSS-induced colitis; Intestinal flora; Lactobacillus johnsonii; Short-chain fatty acids.

外文摘要：Butyrolactone-I (BTL-1), a secondary metabolite from the marine fungus Aspergillus terreus, exhibits numerous biological activities. Previous research has indicated that Butyrolactone-I alleviates intestinal epithelial inflammation via the TLR4/NF-kappa B and MAPK pathways. However, the mechanisms underlying its protection against intestinal barrier damage remain unclear. This study aims to further elucidate these mechanisms. We observed that BTL-1 administration increased the abundance of Lactobacillus johnsonii (LJ) in both in vivo and in vitro experiments, prompting an investigation into the effects of LJ and its metabolites on DSS-induced inflammatory bowel disease (IBD). The results demonstrated that BTL-1 significantly upregulated tight junction (TJ) and adherens junction (AJ) proteins, maintained intestinal barrier integrity, and alleviated DSS-induced IBD in mice. These effects were associated with the proliferation of LJ and its metabolites, such as butyric and propionic acids, and the inhibition of the MAPK signaling pathway in the colon. Interestingly, administering LJ alone produced a protective effect against DSS-induced IBD similar to that observed with BTL-1. Furthermore, butyric acid, a metabolite of LJ, also upregulated TJ/AJ proteins in intestinal epithelial cells through the MAPK signaling pathway. Our findings suggest that BTL-1 regulates intestinal flora, promotes LJ proliferation, protects intestinal barrier integrity, increases the concentrations of butyric and propionic acids, and ultimately inhibits the activation of the MAPK signaling pathway in mice to alleviate IBD. Therefore, BTL-1 could potentially be used as a natural drug to prevent IBD and maintain intestinal flora balance. We explored how butyrolactone-I exerts a preventive effect on IBD through intestinal bacteria ( Lactobacillus johnsonii). (c) 2024 Elsevier Inc. All rights are reserved, including those for text and data mining, AI training, and similar technologies.