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      Lactobacillus paracasei GMNL-32, Lactobacillus reuteri GMNL-89 and L. reuteri GMNL-263 ameliorate hepatic injuries in lupus-prone mice.

      The British Journal of Nutrition
      Cambridge University Press (CUP)
      GMNL-32 Lactobacillus paracasei GMNL-32, Lactobacillus reuteri GMNL-89, MAPK mitogen-activated protein kinase, Lactobacillus paracasei GMNL-32, Probiotics, GMNL-89 Lactobacillus reuteri GMNL-89, MMP matrix metalloproteinase, TUNEL terminal deoxynucleotidyl transferase dUTP nick end labelling, IKK IκB kinase, Liver disorders, Systemic lupus erythematosus, JNK c-Jun N-terminal kinase, SLE systemic lupus erythematosus, CRP C-reactive protein, Lactobacillus reuteri GMNL-263, iNOS inducible nitric oxide synthase, ERK extracellular signal-regulated kinase, GMNL-263 Lactobacillus reuteri GMNL-263

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          Abstract

          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.

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