Intrahepatic transplantation of adipose-derived stem cells attenuates the progression of non-alcoholic fatty liver disease in rats

Mol Med Rep. 2015 Sep;12(3):3725-3733. doi: 10.3892/mmr.2015.3847. Epub 2015 May 26.

Abstract

Non‑alcoholic fatty liver disease (NAFLD) is one of the major causes of chronic liver injury affecting the general health of various populations. In the present study, adipose tissue‑derived stem cells (ADSCs), which were isolated from the adipose tissues of Sprague‑Dawley rats, were transplanted into the liver of high‑fat‑diet‑induced NAFLD rats via the portal vein to attenuate the disease progression of NAFLD. The results demonstrated that ADSC transplantation reduced the serum levels of alanine aminotransferase, total bilirubin, total cholesterol, triglycerides and fatty acids, and reduced the content of malondialdehyde in the liver homogenates. By contrast, ADSC transplantation caused a significant increase in superoxide dismutase activity. These data suggested that the ADSC transplantation improved the liver function, and reduced lipid metabolism and oxidative stress. In addition, the hepatic pathological changes were decelerated, lipid accumulation was reduced, and serum levels of the pro‑inflammatory factors, tumor necrosis factor‑α and interleukin‑6, were downregulated by the ADSC transplantation. Taken together, transplantation with ADSCs attenuates the disease progression of high‑fat‑diet induced NAFLD, therefore, may offer a potential therapeutic approach for the treatment of NAFLD.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adipose Tissue / cytology*
  • Animals
  • Cells, Cultured
  • Interleukin-6 / blood
  • Lipid Metabolism
  • Liver / pathology*
  • Liver / surgery
  • Male
  • Non-alcoholic Fatty Liver Disease / blood
  • Non-alcoholic Fatty Liver Disease / pathology*
  • Non-alcoholic Fatty Liver Disease / surgery
  • Non-alcoholic Fatty Liver Disease / therapy*
  • Oxidative Stress
  • Rats
  • Rats, Sprague-Dawley
  • Stem Cell Transplantation*
  • Tumor Necrosis Factor-alpha / blood

Substances

  • Interleukin-6
  • Tumor Necrosis Factor-alpha