Maltol attenuates polystyrene nanoplastic-induced enterotoxicity by promoting AMPK/mTOR/TFEB-mediated autophagy and modulating gut microbiota. (1st April 2023)

• Record Type: Journal Article
• Authors: Jin, Ming-hui; Hu, Jun-nan; Zhang, Ming; Meng, Zhaojie; Shi, Guo-ping; Wang, Zi; Li, Wei
• Is Part Of: Environmental pollution. Volume 322(2023)
• Publication Date: 2023-04-01
• Subjects: Maltol -- Polystyrene nanoplastics -- Intestinal injury -- Autophagy -- Apoptosis; PS Polystyrene nanoplastics -- Maltol 3-hydroxy-2-methyl-4-pyrone -- ROS Reactive oxygen species -- DAO Diamine Oxidase -- MMP Mitochondrial membrane potential -- TEM Transmission Electron Microscope -- AB-PAS Alcian blue and Periodic acid Schiff stain -- MTT Methyl-thiazolyl-tetrazolium -- RMSD Root mean square deviation -- RMSF Root mean square fluctuation -- SCFA short-chain fatty acid -- CQ Chloroquine -- AICAR Acadesine; Pollution -- Periodicals; Pollution -- Environmental aspects -- Periodicals; Environmental Pollution -- Periodicals; Pollution -- Périodiques; Pollution -- Aspect de l'environnement -- Périodiques; Pollution -- Effets physiologiques -- Périodiques; Pollution; Pollution -- Environmental aspects; Periodicals; Electronic journals; 363.73
• DOI: 10.1016/j.envpol.2023.121202
• Languages: English
• ISSNs: 0269-7491

Abstract

Abstract: The production and application of nanoplastics has been increased during decades, and the enterotoxicity caused by their bioaccumulation has attracted vast attention. Maltol was proved to exert a protective effect on gut damage induced by carbon tetrachloride and cisplatin, indicating its confrontation with nanoplastics-induced intestinal toxicity. To explore the ameliorative effects of maltol on polystyrene nanoplastics (PS)-mediated enterotoxicity and the underlying mechanism, the mice were exposed to PS (100 mg/kg), combining with or without the treatment of maltol treatment at 50 and 100 mg/kg. We found PS exposure caused intestinal barrier damage and enterocyte apoptosis, while lysosomal dysfunction and autophagic substrate degradation arrest in enterocytes of mice were also observed. In addition, PS exacerbated the disturbance of the intestinal microbial community, affected the abundance of lysosome and apoptosis-related bacterial genes, and decreased the number of known short-chain fatty acid (SCFA) producing bacteria. However, those alterations were improved by the maltol treatment. Maltol also protected the human intestinal Caco-2 cells from PS-induce damages. Mechanistic studies showed maltol promoted TFEB nuclear translocation through the AMPK/mTOR signaling pathway to restore lysosomal function and reduce autophagy dependent apoptosis. The findings in the present work might help to elucidate the potential molecular mechanisms of PS-induced enterotoxicity. For the first time to our knowledge, the protective effect of maltol on PS-induced intestinal injury was studied from multiple perspectives, which provided a potential therapeutic approach for diseases caused by environmental pollution. Graphical abstract: Molecular mechanism of maltol on signaling crosstalk in PS-induced intestinal injury. Image 1 Highlights: PS triggered autophagy-dependent apoptosis and lysosome dysfunction in the colon. PS damaged the intestinal barrier and intestinal microbiota in mice. Maltol might reduce PS-induced intestinal damage by targeting AMPK.