Curcumin triggers apoptosis via upregulation of Bax/Bcl-2 ratio and caspase activation in SW872 human adipocytes

Mol Med Rep. 2015 Jul;12(1):1151-6. doi: 10.3892/mmr.2015.3450. Epub 2015 Mar 6.

Abstract

Induction of adipocyte apoptosis has been postulated as a novel strategy with which to treat obesity. The effects of curcumin, a polyphenol compound, on the apoptotic signaling pathway in SW872 adipocytes were investigated in the present study. The results showed that cell viability decreased following curcumin treatment in a time- and dose-dependent manner. The results from a single-stranded DNA ELISA assay indicated that curcumin causes the number of apoptotic cells to increase in a concentration-dependent manner. In addition, curcumin treatment resulted in an increased expression of Bax, and a decrease in that of of Bcl-2, with a concomitant upregulation of the Bax/Bcl-2 ratio. Curcumin treatment also led to the release of cytochrome c from mitochondria into the cytosol. Similarly, caspase-dependent poly (ADP) ribose polymerase (PARP) cleavage by curcumin was observed in the current study. In conclusion the results indicate that curcumin is an effective therapeutic agent with which to induce apoptosis in adipocytes. This effect is, in part, mediated through the mitochondrial pathway, which involves upregulation of the Bax/Bcl-2 ratio, cytochrome c release, activation of caspase-3 and the cleavage of PARP.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adipocytes / cytology
  • Adipocytes / drug effects*
  • Adipocytes / metabolism
  • Anti-Inflammatory Agents, Non-Steroidal / pharmacology*
  • Anti-Obesity Agents / pharmacology*
  • Apoptosis / drug effects
  • Caspase 3 / genetics*
  • Caspase 3 / metabolism
  • Cell Line
  • Cell Survival / drug effects
  • Curcumin / pharmacology*
  • Cytochromes c / metabolism
  • DNA, Single-Stranded / chemistry
  • DNA, Single-Stranded / metabolism
  • Dose-Response Relationship, Drug
  • Enzyme-Linked Immunosorbent Assay
  • Gene Expression Regulation
  • Humans
  • Mitochondria / drug effects
  • Poly(ADP-ribose) Polymerases / genetics
  • Poly(ADP-ribose) Polymerases / metabolism
  • Proteolysis / drug effects
  • Proto-Oncogene Proteins c-bcl-2 / antagonists & inhibitors
  • Proto-Oncogene Proteins c-bcl-2 / genetics*
  • Proto-Oncogene Proteins c-bcl-2 / metabolism
  • Signal Transduction
  • bcl-2-Associated X Protein / agonists
  • bcl-2-Associated X Protein / genetics*
  • bcl-2-Associated X Protein / metabolism

Substances

  • Anti-Inflammatory Agents, Non-Steroidal
  • Anti-Obesity Agents
  • BAX protein, human
  • BCL2 protein, human
  • DNA, Single-Stranded
  • Proto-Oncogene Proteins c-bcl-2
  • bcl-2-Associated X Protein
  • Cytochromes c
  • Poly(ADP-ribose) Polymerases
  • Caspase 3
  • Curcumin