Hsu Tsai-Ching, Huang Chih-Yang, Liu Chung-Hsien, Hsu Kuo-Ching, Chen Yi-Hsing, Tzang Bor-Show
1Institute of Biochemistry, Microbiology and Immunology,Chung Shan Medical University,Taichung 402,Taiwan, ROC.
4Graduate Institute of Basic Medical Science,China Medical University,Taichung 404,Taiwan, ROC.
Br J Nutr. 2017 Apr;117(8):1066-1074. doi: 10.1017/S0007114517001039. Epub 2017 May 15.
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.
已知益生菌可通过与全身和黏膜免疫细胞以及肠道上皮细胞相互作用来调节宿主免疫。据报道,补充某些益生菌对包括免疫相关疾病在内的各种疾病有效。然而,关于副干酪乳杆菌GMNL - 32(GMNL - 32)、罗伊氏乳杆菌GMNL - 89(GMNL - 89)和罗伊氏乳杆菌GMNL - 263(GMNL - 263)在自身免疫性疾病尤其是系统性红斑狼疮(SLE)管理中的有效性知之甚少。将易患狼疮的动物模型NZB/W F1小鼠口服灌胃GMNL - 32、GMNL - 89或GMNL - 263,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,在NZB/W F1小鼠中补充GMNL - 32、GMNL - 89或GMNL - 263可改善肝脏细胞凋亡和炎症指标,如基质金属蛋白酶 - 9活性以及C反应蛋白和诱导型一氧化氮合酶的表达。此外,在NZB/W F1小鼠中补充GMNL - 32、GMNL - 89或GMNL - 263可通过抑制丝裂原活化蛋白激酶和NF - κB信号通路来降低肝脏IL - 1β、IL - 6和TNF - α蛋白的表达。首次在此呈现的这些发现表明,GMNL - 32、GMNL - 89和GMNL - 263可减轻易患狼疮小鼠的肝脏炎症和细胞凋亡,并可能为SLE病例中的肝脏疾病提供一种替代疗法。