In recent years, bone marrow-derived mesenchymal stem cells (BMSCs) have been demonstrated to exert extensive therapeutic effects on acute liver injury; however, the underlying mechanisms of these effects have remained to be elucidated. The present study focused on the potential antiapoptotic
and proregenerative effects of BMSCs in Dgalactosamine (DGal) and lipopolysaccharide (LPS)induced acute liver injury in rats. An experimental rat acute liver injury model was established by intraperitoneal injection of DGal (400 mg/kg) and LPS (80 µg/kg). BMSCs and an identical
volume of saline were administered via the caudal vein 2 h after the DGal and LPS challenge. Subsequently, the serum samples were collected to detect the levels of alanine aminotransferase and aspartate aminotransferase. Hematoxylin and eosin staining, terminal deoxynucleotidyl transferasemediated
nickend labeling assay and immunohistochemical staining were performed to determine apoptosis, regeneration and histological changes of liver sections. Western blotting and reverse transcriptionquantitative polymerase chain reaction were performed to detect the protein and mRNA expression
levels of fibrinogenlikeprotein 1 (FGL1), phosphorylated signal transducer and activator of transcription 3 (pSTAT3), STAT3 and Bcell lymphoma 2 (Bcl2) and Bcl2 associated X protein (Bax) in liver tissue samples. The results indicated that intravenous transplantation of BMSCs
significantly decreased the levels of alanine aminotransferase and aspartate aminotransferase, and reduced hepatocellular necrosis and inflammatory cell infiltration. Additionally, a terminal deoxynucleotidyl transferasemediated nickend labeling assay and immunohistochemical staining revealed
that BMSC treatment reduced hepatocyte apoptosis and enhanced liver regeneration. Furthermore, Bcl2 expression was increased, whilst the protein expression of Bax was reduced. The expression of FGL1 and pSTAT3 were elevated concurrently with the improvement of liver function. These results
demonstrated that BMSCs may provide a promising potential agent for the prevention of acute liver injury via inhibition of hepatocyte apoptosis and acceleration of liver regeneration. The mechanism may be, a least in part, a consequence of the upregulation of FGL1 expression and the induction
of STAT3 phosphorylation.
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Document Type: Research Article
Department of Infectious Disease, Wenzhou Key Laboratory of Hepatology, Hepatology Institute of Wenzhou Medical University, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, Zhejiang 325000, P.R. China
Department of Orthopedic Surgery, The Second Affiliated Hospital of Wenzhou Medical University, Wenzhou, Zhejiang 325027, P.R. China
Publication date: August 1, 2015
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Molecular Medicine Reports is a monthly, peer-reviewed journal available in print and online, that includes studies devoted to molecular medicine, underscoring aspects including pharmacology, pathology, genetics, neurosciences, infectious diseases, molecular cardiology and molecular surgery. In vitro and in vivo studies of experimental model systems pertaining to the mechanisms of a variety of diseases offer researchers the necessary tools and knowledge with which to aid the diagnosis and treatment of human diseases.
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