Magnolol-induced apoptosis is mediated via the intrinsic pathway with release of AIF from mitochondria in U937 cells

Takamichi Ikai, Yukihiro Akao, Yoshihito Nakagawa, Kenji Ohguchi, Yoshimichi Sakai, Yoshinori Nozawa

Research output: Contribution to journalArticle

17 Citations (Scopus)

Abstract

Magnolol has been reported to have an inhibitory effect on tumor invasion in vitro and in vivo. In this study, we found that treatment with 30 μM magnolol exhibited growth inhibition partly by inducing apoptosis in cultured human leukemia U937 cells and that the apoptosis was induced via the sequential ordering of molecular events; 1) a transient decrease of phosphorylated extracelluar signal-requlated kinase (ERK), 2) translocation of apoptosis inducing factor (AIF) from mitochondria to cytosol concurrent with a decreased membrane potential, and 3) downregulation of bcl-2 protein. Pretreatment of the cells with a pan-caspase inhibitor Z-Val-Ala-Asp-fluoromethyl ketone (Z-VAD-FMK) did not prevent the apoptosis induced by magnolol. These findings indicated that the above-mentioned sequence of intracellular signaling events led to apoptosis in magnolol-treated U937 cells, which was caspase-independent.

Original languageEnglish
Pages (from-to)2498-2501
Number of pages4
JournalBiological and Pharmaceutical Bulletin
Volume29
Issue number12
DOIs
Publication statusPublished - 01-12-2006
Externally publishedYes

All Science Journal Classification (ASJC) codes

  • Pharmacology
  • Pharmaceutical Science

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