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Simultaneous Amelioratation of Colitis and Liver Injury in Mice by Bifidobacterium longum LC67 and Lactobacillus plantarum LC27

机译:长双歧杆菌LC67和植物乳杆菌LC27同时改善小鼠结肠炎和肝损伤

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摘要

Disturbances in the gut microbiota composition are associated with chronic inflammatory diseases of the intestine and the liver. In a preliminary study, Lactobacillus plantarum LC27 and Bifidobacterium longum LC67 could inhibit Escherichia coli growth and lipopolysaccharide-induced NF-κB activation linked to gut inflammation. Here, we investigated their effects on 2,4,6-trinitrobenzesulfonic acid (TNBS)-induced colitis and liver damage in mice. First, oral administration of LC27 or LC67 (1 × 109 CFU/mouse) inhibited TNBS-induced colon shortening [F(5,30) = 100.66, P < 0.05] and myeloperoxidase activity [F(5,30) = 56.48, P < 0.05]. These probiotics restored TNBS-induced disturbance of gut microbiota, leading to the suppression of Proteobacteria to Bacteroidetes ratio and fecal and blood lipopolysaccharide levels. Second, LC27 and LC67 inhibited TNBS-induced NF-κB activation, reversed TNBS-suppressed tight junction protein expression, and restored Th17/Treg balance. Also, treatment with LC27 or LC67 significantly decreased TNBS-induced alanine transaminase [ALT, F(5,30) = 3.50, P < 0.05] and aspartate transaminase [AST, F(5,30) = 12.81, P < 0.05] levels in the blood, as well as t-butylhydroperoxide-induced ALT and AST levels. Finally, the mixture of LC27 and LC67 (0.5 × 109 CFU/mouse, respectively) synergistically attenuated TNBS- or t-butylhydroperoxide-induced colitis and liver damage. The capability of LC27 and LC67 to reverse TNBS-mediated microbiota shift and damage signals suggests that these probiotics may synergistically attenuate colitis and liver injury by alleviating gut microbiota imbalance.
机译:肠道菌群组成的紊乱与肠道和肝脏的慢性炎性疾病有关。在一项初步研究中,植物乳杆菌LC27和长双歧杆菌LC67可以抑制大肠杆菌的生长,并且脂多糖诱导的NF-κB活化与肠道炎症有关。在这里,我们调查了它们对小鼠2,4,6-三硝基苯磺酸(TNBS)引起的结肠炎和肝损伤的影响。首先,口服LC27或LC67(1××10 9 CFU /小鼠)抑制TNBS诱导的结肠缩短[F(5,30)= 100.66,P <0.05]和髓过氧化物酶活性[F( 5,30)= 56.48,P <0.05]。这些益生菌恢复了TNBS诱导的肠道菌群紊乱,从而抑制了变形杆菌与拟杆菌的比例以及粪便和血液中的脂多糖水平。其次,LC27和LC67抑制TNBS诱导的NF-κB活化,逆转TNBS抑制的紧密连接蛋白表达,并恢复Th17 / Treg平衡。此外,用LC27或LC67处理可显着降低TNBS诱导的丙氨酸转氨酶[ALT,F(5,30)= 3.50,P <0.05)和天冬氨酸转氨酶[AST,F(5,30)= 12.81,P <0.05]水平血液中以及叔丁基过氧化氢诱导的ALT和AST水平。最后,LC27和LC67的混合物(分别为0.5××10 9 CFU /小鼠)可协同减轻TNBS或叔丁基过氧化氢诱发的结肠炎和肝损伤。 LC27和LC67逆转TNBS介导的微生物群移位和破坏信号的能力表明,这些益生菌可以通过减轻肠道菌群失衡来协同减轻结肠炎和肝损伤。

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