TY - JOUR
T1 - Armillaria mellea component armillarikin induces apoptosis in human leukemia cells
AU - Chen, Yu Jen
AU - Wu, Szu-Yuan
AU - Chen, Chien Chih
AU - Tsao, Yu Lin
AU - Hsu, Nai Chi
AU - Chou, Yu Chi
AU - Huang, Huey Lan
N1 - Funding Information:
We thank Dr. King-Song Jeng for reagents and use of equipment. This work was supported by grants MMH-9900-01 and MMH-9875 from Mackay Memorial Hospital , and Grants NSC 98-2314-B-195-005-MY3 , NSC 97-2314-B-309-003 - and NSC 100-2314-B-309-004 - from the National Science Council of Taiwan, ROC .
PY - 2014
Y1 - 2014
N2 - Honey mushroom Armillaria mellea, a commonly used medicinal food in Asia, is an important component of traditional Chinese medicine "Tien-ma". Armillarikin is a compound isolated from A. mellea with unclear biomedical functions. In this study, we found that armillarikin inhibited the viability of human leukemia K562, U937, and HL-60 cells in a concentration-dependent manner, causing cell death mainly attributable to apoptosis accompanied by reduction of mitochondrial transmembrane potential. Armillarikin induced cleavage of caspase-8, caspase-9, caspase-3, and caspase-3 substrate PARP. Armillarikin-induced growth inhibition and apoptosis were reversed by pan-caspase inhibitor Z-VAD-fmk, indicating a caspase-dependent effect. Moreover, armillarikin increased production of intracellular ROS. Prevention of ROS production attenuated armillarikin-induced apoptosis, suggesting mediation by ROS. In conclusion, armillarikin inhibited growth and induced apoptosis through a mechanism involving mitochondria dysfunction, caspase activation and ROS production in human leukemia K562, U937, and HL-60 cells.
AB - Honey mushroom Armillaria mellea, a commonly used medicinal food in Asia, is an important component of traditional Chinese medicine "Tien-ma". Armillarikin is a compound isolated from A. mellea with unclear biomedical functions. In this study, we found that armillarikin inhibited the viability of human leukemia K562, U937, and HL-60 cells in a concentration-dependent manner, causing cell death mainly attributable to apoptosis accompanied by reduction of mitochondrial transmembrane potential. Armillarikin induced cleavage of caspase-8, caspase-9, caspase-3, and caspase-3 substrate PARP. Armillarikin-induced growth inhibition and apoptosis were reversed by pan-caspase inhibitor Z-VAD-fmk, indicating a caspase-dependent effect. Moreover, armillarikin increased production of intracellular ROS. Prevention of ROS production attenuated armillarikin-induced apoptosis, suggesting mediation by ROS. In conclusion, armillarikin inhibited growth and induced apoptosis through a mechanism involving mitochondria dysfunction, caspase activation and ROS production in human leukemia K562, U937, and HL-60 cells.
KW - Apoptosis
KW - Armillaria mellea
KW - Armillarikin
KW - Leukemia
KW - Reactive oxygen species (ROS)
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U2 - 10.1016/j.jff.2013.10.007
DO - 10.1016/j.jff.2013.10.007
M3 - Article
AN - SCOPUS:84895071518
SN - 1756-4646
VL - 6
SP - 196
EP - 204
JO - Journal of Functional Foods
JF - Journal of Functional Foods
IS - 1
ER -
