Curcumin differentially modulates mRNA profiles in Jurkat T and human peripheral blood mononuclear cells

Bioorg Med Chem. 2003 Mar 20;11(6):1057-63. doi: 10.1016/s0968-0896(02)00461-3.

Abstract

Curcumin, the yellow pigment of the rhizome of Curcuma longa is known to inhibit the transcription factors AP-1, Egr-1, NF-kappaB, c-myc and several important signaling kinases. We therefore investigated the differential effects of curcumin in concentation between 1.5 and 13.6 microM on gene expression in T Jurkat CD4(+) and human peripheral blood mononuclear cells (PBMCs). Relative quantification with reverse transcription real-time PCR (RT-rt-PCR) showed that low concentrations of curcumin significantly down-regulated mitogen-induced granulocyte macrophage colony stimulating factor (GM-CSF) mRNA (3- to 5-fold at 3 microM) in a dose- and time-dependent manner in both cell types. In comparison, the down-regulation of inducible nitric oxide (iNOS) mRNA levels was less pronounced, but interferon gamma (IFN-gamma) mRNA was dose-dependently up-regulated with curcumin concentrations up to 8.2 microM. Cyclin D1 mRNA expression was specifically inhibited in Jurkat T cells and stimulated PBMCs. The transcription factors NF-kappaB and NF-ATc were not affected in PBMCs. Interleukin-2 (IL-2), and-6 (IL-6) mRNAs levels were not influenced markedly by curcumin in stimulated PBMCs, but significantly reduced in stimulated Jurkat T cells. In addition, cytotoxic effects and down-regulation of mRNAs, including p65 and the house-keeping genes could only be measured in Jurkat T cells. These findings confirm previous reports on the anti-neoplastic potential of curcumin and show that this compound differentially modulates the expression profile of Th1 cells and PBMCs.

MeSH terms

  • Cell Survival / drug effects
  • Curcumin / pharmacology*
  • Cytokines / biosynthesis
  • DNA Primers
  • Down-Regulation / drug effects
  • Enzyme-Linked Immunosorbent Assay
  • Humans
  • In Vitro Techniques
  • Interleukin-2 / metabolism
  • Jurkat Cells
  • Mitogens / pharmacology
  • Monocytes / drug effects
  • Monocytes / metabolism*
  • NF-kappa B / biosynthesis
  • NF-kappa B / genetics
  • RNA, Messenger / biosynthesis*
  • Reverse Transcriptase Polymerase Chain Reaction
  • Tetradecanoylphorbol Acetate / pharmacology
  • Transcription Factors / biosynthesis

Substances

  • Cytokines
  • DNA Primers
  • Interleukin-2
  • Mitogens
  • NF-kappa B
  • RNA, Messenger
  • Transcription Factors
  • Curcumin
  • Tetradecanoylphorbol Acetate