Apoptotic effects of Antrodia cinnamomea1The generic name of Antrodia camphorata is currently corrected by Chang and Chou (2004).1 fruiting bodies extract are mediated through calcium and calpain-dependent pathways in Hep 3B cells
Journal
Food and Chemical Toxicology
Journal Volume
44
Journal Volume
44
Journal Issue
8
Journal Issue
8
Pages
1316-1326
Start Page
1316
End Page
1326
ISSN
02786915
Date Issued
2006-08
Author(s)
Abstract
Antrodia cinnamomea is well known in Taiwan as a traditional medicine for treating cancer and inflammation. The purpose of this study was to evaluate the apoptotic effects of ethylacetate extract from A. cinnamomea (EAC) fruiting bodies in Hep 3B, a liver cancer cell line. EAC decreased cell proliferation of Hep 3B cells by inducing apoptotic cell death. EAC treatment increased the level of calcium (Ca2+) in the cytoplasm and triggered the subsequent activation of calpain and caspase-12. EAC also initiated the mitochondrial apoptotic pathway through regulation of Bcl-2 family proteins expression, release of cytochrome c, and activation of caspase-9 in Hep 3B cells. Furthermore, the mitochondrial apoptotic pathway amplified the calpain pathway by Bid and Bax interaction and Ca2+ translocation. We have therefore concluded that the molecular mechanisms during EAC-mediated proliferation inhibition in Hep 3B cells were due to: (1) apoptosis induction, (2) triggering of Ca2+/calpain pathway, (3) disruption of mitochondrial function, and (4) apoptotic signaling being amplified by cross-talk between the calpain/Bid/Bax and Ca2+/mitochondrial apoptotic pathways.
Subjects
Antrodia cinnamomea
Apoptosis
Calcium
Calpain
Hep 3B
SDGs
Other Subjects
acetic acid ethyl ester; antrodia cinnamomea extract; calcium; calpain; caspase 12; caspase 9; cytochrome c; plant extract; protein Bax; protein bcl 2; protein Bid; unclassified drug; Antrodia cinnamomea; apoptosis; article; calcium cell level; cancer cell; cancer inhibition; cell function; cell proliferation; Chinese medicine; controlled study; cytoplasm; drug effect; drug synthesis; enzyme activation; evaluation; fruiting body; gene amplification; gene translocation; human; human cell; liver cancer; mitochondrion; molecular dynamics; protein cross linking; protein expression; protein family; protein protein interaction; regulatory mechanism; signal transduction; Apoptosis; BH3 Interacting Domain Death Agonist Protein; Calcium; Calpain; Carcinoma, Hepatocellular; Caspase 12; Caspases; Cell Line, Tumor; Cell Proliferation; Cytochromes c; Drugs, Chinese Herbal; Endoplasmic Reticulum; Enzyme Activation; Enzyme Inhibitors; Flow Cytometry; Fruit; Humans; Liver Neoplasms; Membrane Potentials; Mitochondrial Membranes; Polyporales; Proto-Oncogene Proteins c-bcl-2; Antrodia; Antrodia cinnamomea; Taiwanofungus camphoratus
Type
journal article