首页> 外文期刊>Journal of Agricultural and Food Chemistry >Lactobacillus plantarum KLDS1.0344 and Lactobacillus acidophilus KLDS1.0901 Mixture Prevents Chronic Alcoholic Liver Injury in Mice by Protecting the Intestinal Barrier and Regulating Gut Microbiota and Liver-Related Pathways
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Lactobacillus plantarum KLDS1.0344 and Lactobacillus acidophilus KLDS1.0901 Mixture Prevents Chronic Alcoholic Liver Injury in Mice by Protecting the Intestinal Barrier and Regulating Gut Microbiota and Liver-Related Pathways

机译:Lactobacillus Plantarum KLDS1.0344和乳杆菌通过保护肠道屏障和调节肠道微生物和肝脏相关途径来防止小鼠中慢性酒精性肝损伤

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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 (Lactobacillus plantarum KLDS1.0344 and Lactobacillus acidophilus 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.
机译:酒精性肝病(ALD)严重损害健康和福祉,尽管之前已经证明一些乳酸菌菌株可以缓解ALD症状,但这些作用背后的机制仍不清楚。在这里,给C57BL/6J小鼠喂食含酒精的Lieber–DeCarli液体饮食6周,以建立慢性酒精性肝损伤模型,以研究乳酸杆菌混合物(植物乳杆菌KLDS1.0344和嗜酸乳杆菌KLDS1.0901)的保护作用和可能机制。结果表明,乳酸菌混合物改善了肠上皮通透性,降低了血清脂多糖(LPS)水平。此外,乳酸杆菌混合物通过调节AMPK、Nrf-2和TLR4/NF-κB途径抑制肝脏脂质积聚、氧化应激和炎症。重要的是,乳酸杆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。综上所述,这些研究结果表明,乳酸杆菌混合物可以积极调节肠道微生物群,导致SCFA水平升高,从而抑制酒精诱导的肝脏脂质积聚和通过肠道-肝脏轴的氧化应激。此外,在施用乳酸杆菌混合物后,肠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,从而抑制酒精诱导的肝脏炎症。

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