首页> 外文期刊>The British Journal of Nutrition >Lactobacillus paracasei GMNL-32, Lactobacillus reuteri GMNL-89 and L. reuteri GMNL-263 ameliorate hepatic injuries in lupus-prone mice
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Lactobacillus paracasei GMNL-32, Lactobacillus reuteri GMNL-89 and L. reuteri GMNL-263 ameliorate hepatic injuries in lupus-prone mice

机译:Lactobacillus paracasei gmnl-32,乳杆菌肠道Gmnl-89和L.Reuterigmnl-263改善狼疮般的小鼠的肝脏伤害

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Probiotics are known to regulate host immunity by interacting with systemic and mucosal immune cells as well as intestinal epithelial cells. Supplementation with certain probiotics has been reported to be effective against various disorders, including immune-related diseases. However, little is known about the effectiveness of Lactobacillus paracasei GMNL-32 (GMNL-32), Lactobacillus reuteri GMNL-89 (GMNL-89) and L. reuteri GMNL-263 (GMNL-263) in the management of autoimmune diseases, especially systemic lupus erythematosus (SLE). NZB/W F1 mice, which are a lupus-prone animal model, were orally gavaged with GMNL-32, GMNL-89 or GMNL-263 to investigate the effects of these Lactobacillus strains on liver injuries in NZB/W F1 mice. The results thus obtained reveal that supplementary GMNL-32, GMNL-89 or GMNL-263 in NZB/W F1 mice ameliorates hepatic apoptosis and inflammatory indicators, such as matrix metalloproteinase-9 activity and C-reactive protein and inducible nitric oxide synthase expressions. In addition, supplementation with GMNL-32, GMNL-89 or GMNL-263 in NZB/W F1 mice reduced the expressions of hepatic IL-1β, IL-6 and TNF-α proteins by suppressing the mitogen-activated protein kinase and NF-κB signalling pathways. These findings, presented here for the first time, reveal that GMNL-32, GMNL-89 and GMNL-263 mitigate hepatic inflammation and apoptosis in lupus-prone mice and may support an alternative remedy for liver disorders in cases of SLE.
机译:已知益生菌通过与全身和粘膜免疫细胞以及肠上皮细胞相互作用来调节宿主免疫。据报道,补充具有某些益生菌的补充是有效对各种疾病,包括免疫相关疾病。然而,关于Lactobacillus ParacilesiGmnL-32(GmnL-32)的有效性,Lactobacillus Reuteri Gmnl-89(Gmnl-89)和L.ReuteriGmnL-263(GmnL-263)的有效性毫无熟悉,在自身免疫疾病的管理中,特别是Systemic Lupus红斑(SLE)。 NZB / W F1小鼠是狼疮易患动物模型,用GMNL-32,GMNL-89或GMNL-263口服致原始,以研究这些乳杆菌菌株对NZB / W F1小鼠肝损伤的影响。由此获得的结果表明,NZB / W F1小鼠中的补充GmnL-32,GmN1-89或GmnL-263改善了肝细胞凋亡和炎症指标,例如基质金属蛋白酶-9活性和C反应蛋白和诱导的一氧化氮合酶表达。此外,通过抑制丝裂原激活的蛋白激酶和NF-,在NZB / W F1小鼠中用GMNL-32,GMNL-89或GMN1-263进行补充,从而减少了肝IL-1β,IL-6和TNF-α蛋白的表达κB信号传导途径。这些发现是第一次在此提出的,揭示了GMNL-32,GMNL-89和GMNL-263减轻了狼疮般的小鼠的肝脏炎症和细胞凋亡,并且可以在SLE的情况下支持肝病的替代补救措施。

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