Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Pivot Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Target Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Query: EC:3.2.1.108 (
lactase
)
2,133
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
Autoimmune hepatitis is a chronic inflammatory disease in the liver with potential to the development of liver fibrosis. Recent evidences suggest that bone marrow derived mesenchymal stem cells (BMSCs) may exert its therapeutic activity through exosomes. Moreover, miR-223 is highly expressed in BMSCs and plays an important role in autoimmune diseases. Therefore, in this study, hepatoprotective role of BMSCs and miR-223 was investigated in both mice and hepatocytes. Liver antigen S100 was used to establish autoimmune hepatitis model in mice while LPS and ATP were used to establish cell injury model in hepatocyte. Before the experiments, BMSCs were infected with pre-miR-223 and transfected with miR-223 inhibitor respectively. Exosomes from bone marrow stem cells were isolated by ultracentrifugation. Liver injury was evaluated by serum levels of ALT and AST as well as liver histology. Inflammation and cell death were examined by inflammatory cytokines and
lactase
dehydrogenase respectively. Both BMSCs-exo and BMSCs-exo
miR-223(+)
significantly reversed either S100 or LPS/ATP induced injury in mice and hepatocytes. Meanwhile, the expressions of cytokines,
NLRP3
and caspase-1 were also downregulated by BMSCs-exo and BMSCs-exo
miR-223(+)
at both protein and mRNA levels in mice and hepatocytes. Moreover, BMSCs-exo
miR-223(-)
reverses the effects of BMSCs-exo and BMSCs-exo
miR-223(+)
in mouse AIH and in hepatocytes. In conclusion, bone marrow stem cell derived exosomes can protect liver injury in an experimental model of autoimmune hepatitis and the mechanism could be related to exosomal miR-223 regulation of
NLRP3
and caspase-1.
...
PMID:BMSCs-derived miR-223-containing exosomes contribute to liver protection in experimental autoimmune hepatitis. 2914 57