Abstract

Transplantation of bone marrow mesenchymal stem cells has attracted more and more attention as a regenerative therapy for the treatment of liver diseases. A large number of studies have shown that this kind of cells can inhibit the activation of hepatic stellate cells and regulate tissue homeostasis and immune system via a variety of ways. Meanwhile, bone marrow mesenchymal stem cells can inhibit apoptosis of hepatocyte, improve liver function, and reduce inflammation through multiple pathways. These cells have a broad prospect in the treatment of liver cirrhosis. At present, there are many studies on the specific mechanism of bone marrow mesenchymal stem cells transplantation in the treatment of liver cirrhosis. This paper reviews the pathogenesis of liver cirrhosis and the mechanism of bone marrow mesenchymal stem cells transplantation in the treatment of liver cirrhosis, discusses the effectiveness of traditional Chinese medicine method in enhancing the efficacy of bone marrow mesenchymal stem cells transplantation, and looks forward to its application prospect in the future.

Highlights

  • Liver cirrhosis is the end stage of chronic liver disease. e progress of chronic liver disease can cause a variety of body damage, such as upper gastrointestinal bleeding, infection, hepatic encephalopathy, hepatocellular carcinoma, hepatorenal syndrome, and other malignant diseases [1]

  • Du et al [24] have studied the therapeutic effect of Bone marrow mesenchymal stem cells (BMSCs) transfected with human matrix metalloproteinase-1 (MMP-1) on carbon tetrachloride-induced hepatic fibrosis in rats. ey suggested that BMSCs may be a potential cell source in preventing liver fibrosis and MMP1 gene may enhance the anti-fibrotic effect of BMSCs. e in vitro studies of Tanimoto et al [25] found that BMSCs inhibit the activation of hepatic stellate cells (HSCs) by regulating the expression of humoral factors and increase matrix metalloproteinases (MMPs)-9, which helps to inhibit activated HSCs and improve fibrosis

  • Chinese Materia Medical can stimulate the proliferation of BMSCs and improve the survival rate of BMSCs, and improve the success rate of mesenchymal stem cell (MSC) differentiating into hepatocyte-like cells (HLCs). e differentiation of MSCs has been seen in two main routes: (1) directly into hepatocytes; (2) induced by cytokines such as hepatocyte growth factor (HGF) that is secreted by MSCs and injured liver tissue

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Summary

Introduction

Liver cirrhosis is the end stage of chronic liver disease. e progress of chronic liver disease can cause a variety of body damage, such as upper gastrointestinal bleeding, infection, hepatic encephalopathy, hepatocellular carcinoma, hepatorenal syndrome, and other malignant diseases [1]. Bone marrow mesenchymal stem cells (BMSCs), of which the genetic background is relatively stable and the use rarely involves ethical problems, can be isolated and greatly expanded in vitro. By using these cells, the implantation reaction in vivo is weak, the rejection of transplantation can be avoided, and its allogeneic cell transplantation does not pose a risk of xenovirus infection. With the flattening of villi on the surface of hepatocytes and the formation of barriers, the transport of substances in hepatic sinusoids through the walls of hepatic sinusoids to hepatocytes was blocked, which interfered with the function of hepatocytes directly, resulting in the dysfunction of synthesis of hepatocytes. e stenosis of hepatic sinusoid, obstruction of blood flow, and increase of intrahepatic resistance affect the hemodynamic of portal vein, cause hypoxia of hepatocytes and disturbance of nutrient supply, aggravate hepatocyte necrosis, and make initiator factors work continuously. e fibre bundle of the portal area and hepatic capsule extend to the central vein of the hepatic lobule. ese fibre septa encircle the regenerated nodules or re-segment the residual hepatic lobules and transform them into pseudo-lobules, forming a typical histopathological morphology of liver cirrhosis

Mechanism of BMSCs in Liver Cirrhosis
Improving BMSCs Differentiating into HLCs
Findings
Conclusions
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