Effect of Yi Guan Jian decoction on differentiation of bone marrow mesenchymalstem cells into hepatocyte-like cells in dimethylnitrosamine-induced liver cirrhosis in mice
| Autor: | Hai‑Long Chen, Ai‑Jing Leng, Yuan Zhang, Yan Xiang, Long‑Qing Lu, Bing‑Yao Pang, Ying Zhu, Qiao‑Ling Xie |
|---|---|
| Jazyk: | angličtina |
| Rok vydání: | 2016 |
| Předmět: |
0301 basic medicine
Cancer Research medicine.medical_specialty Cirrhosis medicine.medical_treatment Cellular differentiation Biochemistry Yi Guan Jian decoction 03 medical and health sciences 0302 clinical medicine Internal medicine Genetics medicine Molecular Biology business.industry Growth factor bone marrow mesenchymal stem cells Articles differentiation medicine.disease Molecular biology 030104 developmental biology medicine.anatomical_structure Endocrinology Oncology 030220 oncology & carcinogenesis Hepatocyte Molecular Medicine Hepatocyte growth factor Liver function Bone marrow Signal transduction business dimethylnitrosamine-induced liver cirrhosis hepatocyte-like cells medicine.drug |
| Zdroj: | Molecular Medicine Reports |
| ISSN: | 1791-3004 1791-2997 |
| Popis: | Yi Guan Jian decoction (YGD) may induce the differentiation of bone marrow mesenchymal stem cells (BMSCs) into hepatocyte-like cells (HLCs); however, the underlying mechanisms remain to be elucidated. The present study aimed to investigate this process. To do this, a dimethylnitrosamine (DMN)-induced liver cirrhosis mouse model was established. The mice from the model group were randomly divided into three subgroups: i) Negative control, ii) hepatocyte growth factor and iii) YGD. The overall health, liver function and histological alterations were monitored. The expression of α‑smooth muscle actin (α‑SMA), C‑X‑C chemokine receptor type 4 (CXCR4), extracellular signal‑regulated kinase (ERK1/2), nuclear factor κB p65 subunit (NF‑κB p65) and β‑catenin were measured by immunohistochemistry, western blotting and reverse transcription‑quantitative polymerase chain reaction. Following administration of DMN, the overall health of the mice significantly decreased, with an increase in pathological developments and liver damage resulting in a decrease in liver function. Immunohistochemistry revealed that the expression of α‑SMA, CXCR4, ERK1/2, NF‑κB p65 and β‑catenin was upregulated. Following treatment with YGD, the overall health, liver function and pathology improved. The mRNA and protein expression levels of CXCR4 and ERK1/2 were upregulated, where as α‑SMA, NF‑κB p65 and β‑catenin levels were downregulated. The results demonstrated that YGD may induce the differentiation of BMSCs into HLCs to reverse DMN‑induced liver cirrhosis; this may be achieved via an upregulation of the SDF‑1/CXCR4 axis to activate the mitogen activated protein kinase/ERK1/2 signaling pathway. |
| Databáze: | OpenAIRE |
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