Atractylenolide III, a sesquiterpenoid, induces apoptosis in human lung carcinoma A549 cells via mitochondria-mediated death pathway

Pharmacological agents that are safe and can sensitize the lung cancer are urgently required. We investigated whether Atractylenolide III (ATL-III), the major component of Atractylodes rhizome can induce apoptosis of the lung carcinoma cells. ATL-III inhibited cell growth, increased lactate dehydrog...

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Bibliographic Details
Published in:Food and chemical toxicology 2011-02, Vol.49 (2), p.514-519
Main Authors: Kang, Tae-Hee, Bang, Ji-Young, Kim, Min-Ho, Kang, In-Cheol, Kim, Hyung-Min, Jeong, Hyun-Ja
Format: Article
Language:English
Subjects:
Antineoplastic Agents, Phytogenic - chemistry
Antineoplastic Agents, Phytogenic - pharmacology
Apoptosis
Apoptosis - drug effects
Apoptosis-inducing factor
Atractylenolide III
Atractylodes
Biological and medical sciences
Carcinoma, Non-Small-Cell Lung - drug therapy
Caspase
Caspase 3 - genetics
Caspase 3 - metabolism
Caspase 9 - genetics
Caspase 9 - metabolism
caspase-3
caspase-9
cell cycle
Cell Cycle - drug effects
cell growth
Cell Line, Tumor
Cytochrome c
death
human umbilical vein endothelial cells
Humans
lactate dehydrogenase
Lactones - chemistry
Lactones - pharmacology
Lung carcinoma cells
lung neoplasms
Lung Neoplasms - drug therapy
Medical sciences
Mitochondria - drug effects
Mitochondria - metabolism
Pneumology
Sesquiterpenes - chemistry
Sesquiterpenes - pharmacology
toxicology
Tumors of the respiratory system and mediastinum
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Summary:Pharmacological agents that are safe and can sensitize the lung cancer are urgently required. We investigated whether Atractylenolide III (ATL-III), the major component of Atractylodes rhizome can induce apoptosis of the lung carcinoma cells. ATL-III inhibited cell growth, increased lactate dehydrogenase release and modulated cell cycle on human lung carcinoma A549 cells. ALT-III induced the activation of caspase-3 and caspase-9 and cleavage of poly-(ADP)-ribose polymerase. ATL-III induced the release of cytochrome c, upregulation of bax expression, and translocation of apoptosis-inducing factor. In addition, ATL-III inhibited the proliferation and capillary tube formation of human umbilical vein endothelial cells. These data indicate that ATL-III is a potential candidate for treatment of human lung carcinoma.
ISSN:0278-6915
1873-6351
DOI:10.1016/j.fct.2010.11.038