Jin Ming-Hui, Hu Jun-Nan, Zhang Ming, Meng Zhaojie, Shi Guo-Ping, Wang Zi, Li Wei
College of Chinese Medicinal Materials, Jilin Provincial International Joint Research Center for the Development and Utilization of Authentic Medicinal Materials, Jilin Agricultural University, Changchun, 130118, China.
College of Life Sciences, Engineering Research Center of the Chinese Ministry of Education for Bioreactor and Pharmaceutical Development, Jilin Agricultural University, Changchun, 130118, China; College of Medicine, Jilin University, Changchun, 130021, China.
Environ Pollut. 2023 Apr 1;322:121202. doi: 10.1016/j.envpol.2023.121202. Epub 2023 Feb 7.
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.
几十年来，纳米塑料的生产和应用不断增加，其生物累积所导致的肠毒性已引起广泛关注。已证明麦芽酚对四氯化碳和顺铂诱导的肠道损伤具有保护作用，表明其可对抗纳米塑料诱导的肠道毒性。为了探究麦芽酚对聚苯乙烯纳米塑料（PS）介导的肠毒性的改善作用及其潜在机制，将小鼠暴露于PS（100 mg/kg），同时分别给予或不给予50 mg/kg和100 mg/kg的麦芽酚处理。我们发现，暴露于PS会导致肠道屏障损伤和肠上皮细胞凋亡，同时还观察到小鼠肠上皮细胞中的溶酶体功能障碍和自噬底物降解停滞。此外，PS加剧了肠道微生物群落的紊乱，影响了溶酶体和凋亡相关细菌基因的丰度，并减少了已知的短链脂肪酸（SCFA）产生菌的数量。然而，麦芽酚处理改善了这些改变。麦芽酚还保护人肠道Caco-2细胞免受PS诱导的损伤。机制研究表明，麦芽酚通过AMPK/mTOR信号通路促进TFEB核转位，以恢复溶酶体功能并减少自噬依赖性凋亡。本研究结果可能有助于阐明PS诱导肠毒性的潜在分子机制。据我们所知，首次从多个角度研究了麦芽酚对PS诱导的肠道损伤的保护作用，为环境污染所致疾病提供了一种潜在的治疗方法。
