肠乳杆菌/鼠李糖乳杆菌可预防afb1诱导的肝损伤:参与肠粘膜屏障

Yuanyuan Chen, Honglin Liu, Tianhui An, Qian Wu, Hongtao Zhang, Juan J. Loor, Jiaxin Cheng, Junqi Wang, Jian Sun
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摘要

黄曲霉毒素B1 (AFB1)是一种广泛传播的真菌毒素,对人类和动物的健康构成威胁。肝脏是afb1诱导损伤的主要靶器官,主要引起炎症损伤和氧化应激。AFB1进入机体后,可破坏肠道屏障功能,其代谢产物被转运到肝脏。因此,肝脏损伤与肠屏障损伤密切相关。乳酸菌通过改善肠道屏障功能,在减轻肝损伤方面起着至关重要的作用。在我们之前的报告中,我们报道了乳酸杆菌减少AFB1引起的肝损伤。然而,目前尚不清楚肠道屏障如何促进乳杆菌对AFB1的保护作用。为了研究肠道乳杆菌/鼠李糖对AFB1诱导的肝损伤的保护作用和肠道屏障机制,我们对雄性SD大鼠口服AFB1和肠道乳杆菌/鼠李糖。分析大鼠体重、脏器指数、肝脏和肠道组织病理变化、肝肾功能指标、肠黏膜屏障指标、血清AFB1含量及炎症因子、肝脏氧化应激指数、短链脂肪酸含量。我们的研究结果表明,暴露于AFB1会导致肝脏组织病理学和生化功能的改变,改变炎症反应和氧化应激,破坏肠黏膜屏障,诱导炎症因子和肝脏炎症的积累。然而,添加肠乳杆菌或鼠李糖乳杆菌可显著预防afb1诱导的肝损伤,通过维持肠粘膜屏障的完整性来减轻组织病理学改变和肝损伤。
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Lactobacillus intestinalis/Lactobacillus rhamnosus protects against AFB1-induced liver damage: involvement of intestinal mucosal barrier
Abstract Aflatoxin B1 (AFB1) is a widely spread mycotoxin that poses a threat to the healthy to human and animals. The liver is the main target organ for AFB1-induced damage, primarily causing inflammatory injury and oxidative stress. When AFB1 enters the body, it can damage the intestinal barrier function, and its metabolites are transported to the liver. Therefore, the damage to the liver is closely associated with intestinal barrier impairment. Lactobacillus plays a crucial role in mitigating liver damage by improving the intestinal barrier function. In our previous report, we reported that Lactobacillus reduces liver damage caused by AFB1. However, it is still unclear how the intestinal barrier contributes to the protective effects of Lactobacillus against AFB1. To investigate the protective effects and intestinal barrier mechanisms of Lactobacillus intestinals /rhamnosus against AFB1-induced liver damage, we orally administered AFB1 and Lactobacillus intestinals/rhamnosus to male SD rats. Then the body weight, organ index, histopathological changes in the liver and gut, liver and kidney function indicators, intestinal mucosal barrier indicators, serum AFB1 content and inflammatory factors, liver oxidative stress index, and short-chain fatty acids content were analyzed. Our findings demonstrate that exposure to AFB1 resulted in changes in liver histopathology and biochemical functions, altered inflammatory response and oxidative stress, compromised the intestinal mucosal barrier, and induced the accumulation of inflammatory factor and inflammation in the liver. However, supplementation with Lactobacillus intestinals or Lactobacillus rhamnosus significantly prevented AFB1-induced liver injury, alleviated histopathological changes and hepatic injury by the maintenance of intestinal mucosal barrier integrity.
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