PDF(Pubmed)
Abstract：
Alcoholic liver damage is caused by long-term or heavy drinking, and it may further progress into alcoholic liver diseases (ALD). Probiotic supplements have been suggested for the prevention or improvement of liver damage. This study was designed to consider the ameliorative effects of Lactobacillus rhamnosus NKU FL1-8 isolated from infant feces against alcoholic liver damage. The mice were gavaged with a 50% ethanol solution and treated with 109 CFU of L. rhamnosus NKU FL1-8 suspension. The factors for liver function, oxidative stress, inflammation, gut microbiota composition, and intestinal barrier integrity were measured. The results showed that L. rhamnosus NKU FL1-8 could decrease the levels of aspartate aminotransferase (AST) to 61% and alanine aminotransferase (ALT) to 50% compared with ethanol given by gavage. It could inhibit the expression level of malondialdehyde (MDA), increase superoxide dismutase (SOD), glutathione (GSH) to relieve oxidative stress, and down-regulate the cytokines to decrease hepatic inflammation. After treatment, the level of triglycerides was reduced, and the expression levels of adenosine 5\'-monophosphate (AMP)-activated protein kinase (AMPK) and the peroxisome proliferators-activated receptor-α (PPAR-α) pathway were up-regulated. Additionally, the 16S rRNA sequencing analysis showed that L. rhamnosus NKU FL1-8 increased the relative abundance of Lactobacillus, Ruminococcaceae, etc. At the same time, L. rhamnosus NKU FL1-8 could significantly reduce lipopolysaccharides (LPS) and enhance intestinal tight junction proteins. These results demonstrated that L. rhamnosus NKU FL1-8 could reduce the level of oxidative stress, fat accumulation, and liver inflammation caused by alcohol in the host. The underlying mechanism could be that L. rhamnosus NKU FL1-8 inhibits LPS by regulating the gut microbiota and repairing the intestinal barrier. Thereby, these findings support L. rhamnosus NKU FL1-8 as a potential functional food for the relief of ALD.
摘要：
酒精性肝损害是由长期或大量饮酒引起的，它可能进一步发展为酒精性肝病（ALD）。益生菌补充剂已被建议用于预防或改善肝损伤。本研究旨在考虑从婴儿粪便中分离的鼠李糖乳杆菌NKUFL1-8对酒精性肝损伤的改善作用。用50%的乙醇溶液给小鼠灌胃,并用109CFU的鼠李糖乳杆菌NKUFL1-8悬浮液处理。肝功能的因素，氧化应激，炎症,肠道菌群组成，和肠屏障完整性进行测量。结果表明，与灌胃乙醇相比，鼠李糖乳杆菌NKUFL1-8可将天冬氨酸转氨酶（AST）水平降低至61％，丙氨酸转氨酶（ALT）水平降低至50％。能抑制丙二醛(MDA)的表达,增加超氧化物歧化酶（SOD），谷胱甘肽（GSH）缓解氧化应激，并下调细胞因子以减少肝脏炎症。治疗后,甘油三酯的水平降低了，5磷酸腺苷（AMP）激活蛋白激酶（AMPK）和过氧化物酶体增殖物激活受体-α（PPAR-α）途径的表达水平上调。此外,16SrRNA测序分析表明，鼠李糖乳杆菌NKUFL1-8增加了乳杆菌的相对丰度，Ruminocycaceae,等。同时,鼠李糖乳杆菌NKUFL1-8能显著减少脂多糖(LPS)和增强肠紧密连接蛋白。这些结果表明鼠李糖乳杆菌NKUFL1-8可以降低氧化应激水平，脂肪堆积,和宿主体内酒精引起的肝脏炎症。潜在的机制可能是鼠李糖乳杆菌通过调节肠道菌群和修复肠道屏障来抑制LPS。因此，这些发现支持鼠李糖乳杆菌NKUFL1-8作为缓解ALD的潜在功能性食物。
