2. Academic Validation
  3. Butyrolactone-I from marine fungi alleviates intestinal barrier damage caused by DSS through regulating lactobacillus johnsonii and its metabolites in the intestine of mice

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

  • J Nutr Biochem. 2024 Oct 22:135:109786. doi: 10.1016/j.jnutbio.2024.109786.
Shengwei Chen 1,  Xueting Niu 1,  Yi Zhang 2,  Jiaying Wen 1,  Minglong Bao 1,  Yin Li 1,  Yuan Gao 1,  Xinchen Wang 1,  Xiaoxi Liu 3,  Yanhong Yong 3,  Zhichao Yu 3,  Xingbing Ma 3,  Jong-Bang Eun 4,  Jae-Han Shim 5,  A M Abd El-Aty 6,  Xianghong Ju 7
Affiliations

Affiliations

  • 1 College of Coastal Agricultural Sciences, Guangdong Ocean University, Zhanjiang, China; Shenzheng Institute of Guangdong Ocean University, Organization X, Shenzheng, China.
  • 2 College of Food Science and Technology, Guangdong Ocean University, Zhanjiang, China.
  • 3 College of Coastal Agricultural Sciences, Guangdong Ocean University, Zhanjiang, China.
  • 4 Department of Food Science and Technology, Chonnam National University, Gwangju, Republic of Korea.
  • 5 Natural Products Chemistry Laboratory, Biotechnology Research Institute, Chonnam National University, Buk-gu, Gwangju, Republic of Korea.
  • 6 Department of Pharmacology, Faculty of Veterinary Medicine, Cairo University, Giza, Egypt; Department of Medical Pharmacology, Medical Faculty, Ataturk University, Erzurum, Turkey.
  • 7 College of Coastal Agricultural Sciences, Guangdong Ocean University, Zhanjiang, China; Shenzheng Institute of Guangdong Ocean University, Organization X, Shenzheng, China. Electronic address: juxh77@163.com.
PMID: 39447992 DOI: 10.1016/j.jnutbio.2024.109786
Abstract

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-κB 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).

Keywords

Butyrolactone-I; DSS-induced colitis; Intestinal flora; Lactobacillus johnsonii; Short-chain fatty acids.

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