Herba houttuyniae extract induces apoptotic death of human promyelocytic leukemia cells via caspase activation accompanied by dissipation of mitochondrial membrane potential and cytochrome c release.
- Author:
Kang Beom KWON
1
;
Eun Kyung KIM
;
Byung Cheul SHIN
;
Eun A SEO
;
Jeong Yeh YANG
;
Do Gon RYU
Author Information
1. Department of Physiology, School of Oriental Medicine, Korea.
- Publication Type:Original Article ; Research Support, Non-U.S. Gov't
- Keywords:
apoptosis;
cancer;
caspase;
medicine;
her-bal;
mitochondria;
phytotherapy
- MeSH:
Apoptosis/*drug effects;
Caspases/*metabolism;
Cytochrome c Group/*metabolism;
Enzyme Activation/drug effects;
HL-60 Cells;
Human;
Medicine, Oriental Traditional;
Membrane Potentials/drug effects;
Mitochondria/*drug effects;
Plant Extracts/*pharmacology;
Plants, Medicinal/*chemistry
- From:Experimental & Molecular Medicine
2003;35(2):91-97
- CountryRepublic of Korea
- Language:English
-
Abstract:
Herba houttuyniae has been used as a constituent of herval medicine prescriptions for the treatment of inflammation, cancer, and other diseases. In the present study, we investigated the cellular effects of herba houttuyniae extract (HHE) and the signal pathways of HHE-induced apoptosis in HL-60 human promyelocytic leukemia cell line. HHE treatment caused apoptosis of cells as evidenced by discontinuous fragmentation of DNA, the loss of mitochondrial membrane potential, release of mitochondrial cytochrome c into the cytosol, activation of procaspase-9 and caspase-3, and proteolytic cleavage of poly(ADP-ribose) polymerase. Pretreatment of Ac-DEVD-CHO, caspase-3 specific inhibitor, or cyclosporin A, a mitochondrial permeability transition inhibitor, completely abolished HHE-induced DNA fragmentation. Together, these results suggest that HHE possibly causes mitochondrial damage leading to cytochrome c release into cytosol and activation of caspases resulting in PARP cleavage and execution of apoptotic cell death in HL-60 cells.
