Magnesium isoglycyrrhizinate attenuates nonalcoholic fatty liver disease by strengthening intestinal mucosal barrier.

BACKGROUND: Non-alcoholic fatty liver disease (NAFLD)/nonalcoholic steatohepatitis (NASH) has recently risen to the top spot among chronic liver diseases in the world. However, there are no recognized treatments for it. Magnesium isoglycyrrhizate (MgIG) has potential as a NAFLD/NASH therapy. AIMS: To investigate the efficacy of MgIG in improving NAFLD/NASH and the possible pathways and mechanisms. METHODS: C57bl/6 mice were fed a high-fat diet (HFD) and 1 % dextran sulfate sodium (DSS) for 12 weeks to establish the NAFLD/NASH model. MgIG was administered by gavage during the last 7 weeks. First, the therapeutic effects of MgIG on hepatic steatosis and fibrosis, liver injury, and inflammation in the NAFLD/NASH mice were evaluated. Second, liver oxidative stress and hepatocyte apoptosis were detected. Finally, the effect of MgIG on intestinal permeability and short-chain fatty acid (SCFA) levels in mice's intestinal contents were examined. RESULTS: MgIG administration attenuated HFD-induced hepatic steatosis and fibrosis, improved serum biochemical and NAFLD/NASH mice, reduced liver oxidative stress and hepatocyte apoptosis, improved intestinal permeability, and increased fecal SCFA levels in NAFLD/NASH mice. CONCLUSION: MgIG protects against HFD-induced NAFLD/NASH through multiple pathways as well as mechanisms and holds promise as a potentially effective treatment for NAFLD/NASH.

[Construction and identification of mouse wildtype-syndecan-1 and unshedding-syndecan-1 expressing vector].

AIM: To construct the expressing vector pcDNA3.0- wildtype-syndecan-1(WT-sdc1) and pcDNA3.0-unshedding-syndecan-1(uS-sdc1), and to explore the expression in vitro. METHODS: (1)The mouse WT-sdc1 DNA was successfully amplified by PCR and then cloned into pcDNA3.0. uS-sdc1 was construct by Gene splicing by overlap extension- PCR on the basis of WT-sdc1. The two vectors confirmed by DNA sequencing. (2)there are 4 groups in our research: control group, pcDNA3.0 transfected group, WT-sdc1 transfected group and uS-sdc1 transfected group. each vecter was transfected into IEC-6 cells by Lipofectamine(TM);2000. RT-PCR, Western blot and Dot blot were performed to detect the expression of syndecan-1 before and after stimulation of phorbol 12-myristate 13-acetate (PMA) for 15 min. RESULTS: The vector WT-sdc1 and uS-sdc1 were successfully constructed although an non-sense mutation was in uS-sdc1. Compared to control and pcDNA3.0 transfected groups, WT-sdc1 and uS-sdc1 groups showed a significant increase in the expression of syndecan-1 in both mRNA and protein levels. In response to the stimulation of PMA, the expression of syndecan-1 was down-regulated at the protein levels but not mRNA levels. CONCLUSION: The WT-sdc1 and uS-sdc1 are successfully constructed, which lays the foundation for further studying of syndecan-1 in gastrointestinal inflammation.