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

作者：Kim Kil Nam; Ham Young Min; Moon Ji Young; Kim Min Jin; Jung Yong Hwan; Jeon You Jin; Lee Nam Ho; Kang Nalae; Yang Hye Mi; Kim Daekyung^*; Hyun Chang Gu

来源：Food Chemistry, 2012, 135(3): 2112-2117.

DOI：10.1016/j.foodchem.2012.05.067

• Acanthopanax koreanum
• Acanthoic acid (ACAN)
• Apoptosis
• HL-60 cells
• Mitogen-activated protein kinase (MAPK)

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.

• 出版日期2012-12-1