[Therapeutic efficacy of bone marrow-derived mesenchymal stem cells infused into mice with liver injury induced by concanavalin A]

Zhongguo Shi Yan Xue Ye Xue Za Zhi. 2009 Oct;17(5):1289-93.
[Article in Chinese]

Abstract

The aim of this study was to evaluate the therapeutic potential of bone marrow mesenchymal stem cells (MSC) on acute liver injury induced by concanavalin A (ConA). MSCs were isolated from male C57BL/6 mice and cultured, and a ConA-induced acute liver injury model was used. MSCs were systemically infused immediately after mice were challenged with ConA, control mice received only saline infusion. 24 hours after MSC transplantation, the level of serum aminotransferases, histologic change and in situ apoptosis of cells were detected, the expression of inflammatory mediators were examined by real-time RT-PCR. The results indicated that MSC transplantation significantly reduced ConA-induced acute liver injury, including the decrease of the level of serum alanine aminotransferase (ALT), serum aspartate aminotransferase (AST) and the extenuation of liver necrosis and in situ apoptosis. Furthermore, after MSC infusion the expression of TNF-alpha, IFN-gamma in liver decreased greatly (p<0.05) with no statistical difference in the expression of iNOS, IL-2 and IL-10 (p>0.05). It is concluded that the systemic infusion of MSCs can alleviate ConA induced acute liver injury in mice.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Bone Marrow Cells / cytology
  • Chemical and Drug Induced Liver Injury / therapy*
  • Concanavalin A / adverse effects*
  • Interferon-gamma / metabolism
  • Interleukin-10 / metabolism
  • Interleukin-2 / metabolism
  • Liver / pathology
  • Male
  • Mesenchymal Stem Cell Transplantation*
  • Mice
  • Mice, Inbred C57BL
  • Nitric Oxide Synthase Type II / metabolism
  • Treatment Outcome
  • Tumor Necrosis Factor-alpha / metabolism

Substances

  • IL10 protein, mouse
  • Interleukin-2
  • Tumor Necrosis Factor-alpha
  • Concanavalin A
  • Interleukin-10
  • Interferon-gamma
  • Nitric Oxide Synthase Type II
  • Nos2 protein, mouse