Rosmarinic acid failed to suppress hydrogen peroxide-mediated apoptosis but induced apoptosis of Jurkat cells which was suppressed by Bcl-2

Evangelos Kolettas, Christoforos Thomas, Eleni Leneti, Ioannis Skoufos, Christina Mbatsi, Christina Sisoula, George Manos, Angelos Evangelou

Research output: Contribution to journalArticlepeer-review

20 Scopus citations

Abstract

Rosmarinic acid (RosA), frequently found as a secondary metabolite in herbs and medicinal plants, has exhibited antioxidative and anti-inflammatory activities. RosA was shown to inhibit the proliferation and induce apoptosis of Jurkat T cells but the mechanism of action of RosA in apoptosis remains elusive. RosA inhibited the proliferation of Jurkat cells in a dose-dependent manner by suppressing the expression of cyclin D3 and p21Cip1/Waf1 and up-regulating p27Kip1. RosA induced apoptosis of Jurkat cells in a dose-dependent manner and failed to protect them from hydrogen peroxide (H2O2)-mediated apoptosis. Induction of apoptosis by RosA correlated with suppression of Bcl-2 but not of Bak or PUMA. Overexpression of Bcl-2 protected Jurkat cells from both H2O2- and RosA-induced apoptosis by altering the ratio of anti- to pro-apoptotic members of the Bcl-2 family. In conclusion, RosA inhibited Jurkat cell proliferation by altering the expression of cyclins and cyclin-dependent kinase inhibitors and induced apoptosis most likely acting through the mitochondrial pathway and possessed no anti-oxidant properties.

Original languageEnglish (US)
Pages (from-to)111-120
Number of pages10
JournalMolecular and Cellular Biochemistry
Volume285
Issue number1-2
DOIs
StatePublished - Apr 2006

Keywords

  • Apoptosis
  • Bcl-2 members
  • Hydrogen peroxide
  • Proliferation
  • Rosmarinic acid

ASJC Scopus subject areas

  • Molecular Biology
  • Clinical Biochemistry
  • Cell Biology

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