Yijing Cai1, Zhuolin Zou1, Liyuan Liu1, Si Chen1, Yi Chen1, Zhuo Lin2, Keqing Shi3, Lanman Xu3, Yongping Chen1. 1. Department of Infection Diseases, The First Affiliated Hospital of Wenzhou Medical University Wenzhou, Zhejiang 325000, P.R. China ; Wenzhou Key Laboratory of Hepatology Wenzhou, Zhejiang 325000, P.R. China ; Hepatology Institute of Wenzhou Medical University Wenzhou, Zhejiang 325000, P.R. China. 2. Wenzhou Key Laboratory of Hepatology Wenzhou, Zhejiang 325000, P.R. China ; Hepatology Institute of Wenzhou Medical University Wenzhou, Zhejiang 325000, P.R. China. 3. Department of Infection Diseases, The First Affiliated Hospital of Wenzhou Medical University Wenzhou, Zhejiang 325000, P.R. China.
Abstract
OBJECTIVE: To investigate the protective effect of bone marrow-derived mesenchymal stem cells (BMSCs) transplantation on acute liver injury (ALI) rats. MATERIAL AND METHODS: BMSCs were extracted from rat bone marrow, cultured and expansion in vitro, and identified by flow cytometer. Rat model with acute liver injury was established by employing D-galactosamine and Lipopolysaccharide. Male rats were randomly divided into ALI model group and BMSCs transplantation group. Rats were sacrificed 24 h, 72 h and 120 h after BMSCs injection to determine alanine aminotransferase (ALT) and aspartate aminotransferase (AST) levels in serum. Proliferating cell nuclear antigen (PCNA) immunohistochemistry staining and quantitative reverse transcription polymerase chain reaction (RT-PCR) of α-fetoprotein (AFP) and glypican-3 (GPC3) were performed to analysis proliferation. Terminal deoxynucleontidyl Transferase Biotin-dUTP Nick End Labeling (TUNEL) assays were used to analyze apoptosis and mitochondria-dependent-pathway related factors Bax and Bcl-2 were examined by Western blot. RESULTS: Compared with the ALI model group, the BMSCs transplantation group presented the lower levels of ALT, AST, decreased Bax proteins expression, and increased Bcl-2 expression. The mRNA levels of AFP and GPC3 and expression of PCNA were significantly higher in BMSCs transplantation group. CONCLUSIONS: BMSCs transplantation could significantly restore liver function. These effects were supposed to be mediated by suppressing hepatocyte apoptosis as well as promoting proliferation. Reduction of apoptosis seemed to correlate with mitochondria-dependent-pathway.
OBJECTIVE: To investigate the protective effect of bone marrow-derived mesenchymal stem cells (BMSCs) transplantation on acute liver injury (ALI) rats. MATERIAL AND METHODS: BMSCs were extracted from rat bone marrow, cultured and expansion in vitro, and identified by flow cytometer. Rat model with acute liver injury was established by employing D-galactosamine and Lipopolysaccharide. Male rats were randomly divided into ALI model group and BMSCs transplantation group. Rats were sacrificed 24 h, 72 h and 120 h after BMSCs injection to determine alanine aminotransferase (ALT) and aspartate aminotransferase (AST) levels in serum. Proliferating cell nuclear antigen (PCNA) immunohistochemistry staining and quantitative reverse transcription polymerase chain reaction (RT-PCR) of α-fetoprotein (AFP) and glypican-3 (GPC3) were performed to analysis proliferation. Terminal deoxynucleontidyl Transferase Biotin-dUTP Nick End Labeling (TUNEL) assays were used to analyze apoptosis and mitochondria-dependent-pathway related factors Bax and Bcl-2 were examined by Western blot. RESULTS: Compared with the ALI model group, the BMSCs transplantation group presented the lower levels of ALT, AST, decreased Bax proteins expression, and increased Bcl-2 expression. The mRNA levels of AFP and GPC3 and expression of PCNA were significantly higher in BMSCs transplantation group. CONCLUSIONS: BMSCs transplantation could significantly restore liver function. These effects were supposed to be mediated by suppressing hepatocyte apoptosis as well as promoting proliferation. Reduction of apoptosis seemed to correlate with mitochondria-dependent-pathway.
Entities:
Keywords:
Bone marrow-derived mesenchymal stem cells; acute liver injury; apoptosis
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