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β‐Eudesmol Induces JNK‐Dependent Apoptosis through the Mitochondrial Pathway in HL60 Cells
Author(s) -
Li Yanchun,
Li Te,
Miao Caixia,
Li Jianchun,
Xiao Wei,
Ma Enlong
Publication year - 2013
Publication title -
phytotherapy research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.019
H-Index - 129
eISSN - 1099-1573
pISSN - 0951-418X
DOI - 10.1002/ptr.4727
Subject(s) - apoptosis , hl60 , biology , dna fragmentation , cytochrome c , cytotoxic t cell , kinase , microbiology and biotechnology , downregulation and upregulation , mitochondrion , poly adp ribose polymerase , caspase 3 , mitochondrial apoptosis induced channel , fragmentation (computing) , bcl 2 family , caspase , programmed cell death , biochemistry , in vitro , polymerase , dna , ecology , gene
β‐eudesmol, a natural sesquiterpenol present in a variety of Chinese herbs, is known to inhibit the proliferation of human tumor cells. However, the molecular mechanisms of the effect of β‐eudesmol on human tumor cells are unknown. In the present study, we report the cytotoxic effect of β‐eudesmol on the human leukemia HL60 cells and its molecular mechanisms. The cytotoxic effect of β‐eudesmol on HL60 cells was associated with apoptosis, which was characterized by the presence of DNA fragmentation. β‐eudesmol‐induced apoptosis was accompanied by cleavage of caspase‐3, caspase‐9, and poly (ADP‐ribose) polymerase; downregulation of Bcl‐2 expression; release of cytochrome c from mitochondria; and decrease in mitochondrial membrane potential (MMP). Activation of c‐Jun N‐terminal kinases (JNK) mitogen‐activated protein kinases was observed in β‐eudesmol‐treated HL60 cells, and the inhibitor of JNK blocked the β‐eudesmol‐induced apoptosis, downregulation of Bcl‐2, and the loss of MMP. These data suggest that β‐eudesmol induces apoptosis in HL60 cells via the mitochondrial apoptotic pathway, which is controlled through JNK signaling. Copyright © 2012 John Wiley & Sons, Ltd.