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首页> 外文期刊>Journal of Functional Foods >Lactobacillus breuis OK56 ameliorates high-fat diet-induced obesity in mice by inhibiting NF-kappa B activation and gut microbial LPS production
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Lactobacillus breuis OK56 ameliorates high-fat diet-induced obesity in mice by inhibiting NF-kappa B activation and gut microbial LPS production

机译:布氏乳杆菌OK56通过抑制NF-κB活化和肠道微生物LPS的产生来改善高脂饮食诱导的小鼠肥胖

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摘要

The anti-obesity effects of anti-inflammatory probiotics, isolated Lactobacillus brevis OK56 from the kimchi lactic acid bacteria collection, were examined and its effects on high-fat diet (HFD)-induced obesity (DIO) mice were evaluated. OK56 strongly inhibited NF-kappa B activation and TNF-alpha, IL-1 beta, and IL-6 expression in lipopolysaccharide (LPS)-stimulated macrophages. Oral administration of OK56 (1 x 10(9) CPU/mouse) suppressed the HFD-induced increase in body and epididymal fat weight gains (by 28 and 31%, respectively), as well as plasmatic atherogenic index, and LPS level. Real-time PCR analysis revealed that OK56 also inhibited HFD-induced expression of F4/80, CD68, CD204,TNF-alpha, and IL-1 beta in the adipose tissue of DIO mice. OK56 abrogated the HFD-induced disturbance to gut microbiota, such as the reduction in the number of bifidobacteria, the increase in the colonic fluid LPS, and the increase in the breath H-2 levels. OK56 also inhibited HFD-induced expression of inducible NO synthetase (iNOS) and cyclooxygenase (COX)-2 and the activation of nuclear factor (NF)-kappa B in the colon. Furthermore, OK56 inhibited HFD-reduced expression of tight junction proteins ZO-1, occludin and claudin-1. These results suggest that OK56 has anti-obesity, which exerts through the inhibition of gut microbiota LPS production, colonic NF-kappa B signaling pathway, and macrophage infiltration into the adipose tissue. (C) 2014 Elsevier Ltd. All rights reserved.
机译:检查了抗炎益生菌(从泡菜乳酸菌集合中分离出的短乳杆菌OK56)的抗肥胖作用,并评估了其对高脂饮食(HFD)诱导的肥胖(DIO)小鼠的作用。 OK56强烈抑制脂多糖(LPS)刺激的巨噬细胞中NF-κB的活化以及TNF-alpha,IL-1 beta和IL-6的表达。口服OK56(1 x 10(9)CPU /小鼠)抑制了HFD诱导的机体和附睾脂肪重量增加(分别降低28%和31%)以及血浆动脉粥样硬化指数和LPS水平。实时PCR分析表明,OK56还抑制了DIO小鼠脂肪组织中HFD诱导的F4 / 80,CD68,CD204,TNF-α和IL-1β的表达。 OK56消除了HFD对肠道菌群的干扰,例如双歧杆菌数量的减少,结肠液LPS的增加以及呼吸H-2水平的增加。 OK56还抑制结肠中HFD诱导的诱导型一氧化氮合酶(iNOS)和环氧合酶(COX)-2的表达以及核因子(NF)-κB的激活。此外,OK56抑制了HFD减少的紧密连接蛋白ZO-1,occludin和claudin-1的表达。这些结果表明,OK56具有抗肥胖作用,其通过抑制肠道微生物群LPS的产生,结肠NF-κB信号通路和巨噬细胞浸润到脂肪组织中发挥作用。 (C)2014 Elsevier Ltd.保留所有权利。

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