Aloe-emodin inhibits adipocyte differentiation and maturation during in vitro human mesenchymal stem cell adipogenesis

J Biochem Mol Toxicol. 2012 Aug;26(8):291-300. doi: 10.1002/jbt.21415. Epub 2012 May 29.

Abstract

In this study, we examined the effects of Aloe-emodin (AE) on the inhibition of adipocyte differentiation during 3-isobutyl-1-methylxanthine (IBMX)-induced adipocyte differentiation in human mesenchymal stem cells (hMSCs). AE treatment (5, 10, and 20 µM) of preadipocyte cells resulted in a significant (p < 0.05) decrease in glycerol phosphate dehydrogenase and triglyceride levels as well as an increase in lactate dehydrogenase activity and attenuated lipid accumulation compared with untreated differentiated adipocytes. Using quantitative reverse transcription polymerase chain reaction, we studied the mRNA expression levels of resistin, adiponectin, aP(2), lipoprotein lipase, PPARγ, and tumor necrosis factor-α in hMSCs undergoing adipocyte differentiation; treatment with AE decreased the expression of these adipogenic genes and decreased adipocyte differentiation. In addition, AE suppresses the differentiation of hMSCs into adipocytes by downregulating PPARγ and C/EBPα expressions. AE significantly inhibited hMSCs proliferation and preadipocyte differentiation within the first 2 days of treatment, indicating that the antiadipogenic effect.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adipocytes / drug effects
  • Adipocytes / metabolism*
  • Adipogenesis / drug effects*
  • Aloe / chemistry*
  • Anthraquinones / pharmacology*
  • Antigens, Differentiation / genetics
  • Antigens, Differentiation / metabolism
  • Cell Survival / drug effects
  • Cells, Cultured
  • Down-Regulation / drug effects
  • Gene Expression / drug effects
  • Humans
  • Lipid Metabolism
  • Mesenchymal Stem Cells / drug effects*
  • Mesenchymal Stem Cells / physiology
  • PPAR gamma / genetics
  • PPAR gamma / metabolism
  • Phenotype
  • Plant Extracts / pharmacology*
  • Triglycerides / metabolism
  • Tumor Necrosis Factor-alpha / genetics
  • Tumor Necrosis Factor-alpha / metabolism

Substances

  • Anthraquinones
  • Antigens, Differentiation
  • PPAR gamma
  • Plant Extracts
  • Triglycerides
  • Tumor Necrosis Factor-alpha
  • aloe emodin