RESUMO
Following the publication of the above article, an interested reader to the authors' attention that there appeared to be several duplications of data panels featured within Figs. 13. After having consulted their original data, the authors have realized that a number of the data panels were inadvertently assembled incorrectly in these figures. The corrected versions of Fig. 1A (showing the correct data for the NC2W and NC4W experiments), Fig. 1B (including the correct data for the C4W, M2W, NC2W and NC4W experiments), Fig. 2 (showing the correct data for the YGD2W experiment), Fig. 3A (NC3W data panel corrected), Fig. 3B (HGF1W and NC3W data panels corrected) and Fig. 3C (C4W data panel corrected) are shown on the next four pages. All these corrections were approved by all authors. The authors regret that these errors were not resolved before the publication of the paper, thank the Editor of Molecular Medicine Reports for granting them the opportunity to publish this corrigendum, and apologize to the readership for any inconvenience caused. [the original article was published in Molecular Medicine Reports 15: 613626, 2017; DOI: 10.3892/mmr.2016.6083].
RESUMO
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 αsmooth muscle actin (αSMA), CXC chemokine receptor type 4 (CXCR4), extracellular signalregulated kinase (ERK1/2), nuclear factor κB p65 subunit (NFκB p65) and ßcatenin were measured by immunohistochemistry, western blotting and reverse transcriptionquantitative 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 αSMA, CXCR4, ERK1/2, NFκB p65 and ßcatenin 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 αSMA, NFκB p65 and ßcatenin levels were downregulated. The results demonstrated that YGD may induce the differentiation of BMSCs into HLCs to reverse DMNinduced liver cirrhosis; this may be achieved via an upregulation of the SDF1/CXCR4 axis to activate the mitogen activated protein kinase/ERK1/2 signaling pathway.