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KLDS1.0344 和 KLDS1.0901 混合物通过保护肠道屏障和调节肠道微生物群及肝脏相关途径来预防小鼠慢性酒精性肝损伤。

KLDS1.0344 and KLDS1.0901 Mixture Prevents Chronic Alcoholic Liver Injury in Mice by Protecting the Intestinal Barrier and Regulating Gut Microbiota and Liver-Related Pathways.

机构信息

College of Food Science, Northeast Agricultural University, Harbin 150030, Heilongjiang, China.

School of Food Science and Technology, Jiangnan University, Wuxi 214122, China.

出版信息

J Agric Food Chem. 2021 Jan 13;69(1):183-197. doi: 10.1021/acs.jafc.0c06346. Epub 2020 Dec 22.

DOI:10.1021/acs.jafc.0c06346
PMID:33353302
Abstract

Health and wellbeing are significantly impaired by alcoholic liver disease (ALD), and although some lactic acid bacteria strains have been shown previously to relieve ALD symptoms, the mechanisms behind these effects are still unclear. Here, the Lieber-DeCarli liquid diet containing alcohol was fed to C57BL/6J mice for 6 weeks to build a chronic alcoholic liver lesion model to study the protective effects and possible mechanisms of Lactobacillus mixture ( KLDS1.0344 and KLDS1.0901). The results showed that Lactobacillus mixture improved intestinal epithelial permeability and reduced the serum lipopolysaccharide (LPS) levels. Furthermore, Lactobacillus mixture inhibited liver lipid accumulation, oxidative stress, and inflammation by regulating AMPK, Nrf-2, and TLR4/NF-κB pathways. Importantly, the Lactobacillus mixture modulated the gut microbiota, resulting in increased short-chain fatty acid (SCFA) producers and decreased Gram-negative bacteria. Taken together, these findings indicated that the Lactobacillus mixture could positively regulate the gut microbiota, causing increased levels of SCFAs, which inhibited alcohol-induced liver lipid accumulation and oxidative stress through the gut-liver axis. Moreover, following administration of the Lactobacillus mixture, the improvement of intestinal epithelial permeability and the reduction of Gram-negative bacteria led to the decrease of LPS entering the portal vein, thereby inhibiting alcohol-induced liver inflammation.

摘要

酒精性肝病 (ALD) 显著损害健康和幸福感,尽管先前已经证明某些乳酸杆菌菌株可以缓解 ALD 症状,但这些效果背后的机制仍不清楚。在这里,使用含有酒精的 Lieber-DeCarli 液体饮食喂养 C57BL/6J 小鼠 6 周,以建立慢性酒精性肝损伤模型,研究乳酸菌混合物 (KLDS1.0344 和 KLDS1.0901) 的保护作用和可能的机制。结果表明,乳酸菌混合物改善了肠道上皮通透性,降低了血清脂多糖 (LPS) 水平。此外,乳酸菌混合物通过调节 AMPK、Nrf-2 和 TLR4/NF-κB 途径抑制肝脂质积累、氧化应激和炎症。重要的是,乳酸菌混合物调节了肠道微生物群,导致短链脂肪酸 (SCFA) 产生菌增加,革兰氏阴性菌减少。总之,这些发现表明,乳酸菌混合物可以通过调节肠道微生物群,增加 SCFA 的水平,从而通过肠-肝轴抑制酒精引起的肝脂质积累和氧化应激,积极调节肠道微生物群。此外,在给予乳酸菌混合物后,肠道上皮通透性的改善和革兰氏阴性菌的减少导致进入门静脉的 LPS 减少,从而抑制酒精引起的肝炎症。

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