Acanthoic acid induces cell apoptosis through activation of the p38 MAPK pathway in HL-60 human promyelocytic leukaemia

  • Food Chem. 2012 Dec 1;135(3):2112-7. doi: 10.1016/j.foodchem.2012.05.067.
Kil-Nam Kim  1 ,  Young Min Ham ,  Ji-Young Moon ,  Min-Jin Kim ,  Yong-Hwan Jung ,  You-Jin Jeon ,  Nam Ho Lee ,  Nalae Kang ,  Hye-Mi Yang ,  Daekyung Kim ,  Chang-Gu Hyun
Affiliations
  • 1. Jeju center, Korea Basic Science Institute (KBSI), Jeju 690-140, Republic of Korea.
PMID: 22953963 DOI: 10.1016/j.foodchem.2012.05.067
Abstract

The present study was designed to evaluate the molecular mechanisms of the action of acanthoic acid (ACAN) from Acanthopanax koreanum (Araliaceae) against HL-60 human promyelocytic leukaemia cells. ACAN reduced the proliferation of HL-60 cells in a dose- and time-dependent manner accompanied by the induction of Apoptosis. Possible mechanisms of ACAN-induced Apoptosis were also examined. The results showed that ACAN-induced the phosphorylation of members of the mitogen-activated protein kinase (MAPK) family, c-Jun N-terminal kinase (JNK), p38 MAPK (p38), and extracellular signal-regulated kinase (ERK). A specific p38 MAPK Inhibitor (SB203580) significantly blocked ACAN-induced Apoptosis and cell viability, whereas an ERK Inhibitor (PD98059) and JNK Inhibitor (SP600125) had no effect. Moreover, ACAN induced the cleavage of Caspase-3 and poly-ADP-ribose polymerase (PARP), and decreased the level of Bcl-xL, but these effects were inhibited by SB203580 pre-treatment. These results strongly suggest that ACAN may have Cancer chemopreventive and therapeutic potential, due to its ability to activate the p38 MAPK-mediated signalling pathways.

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