Molecular mechanism of apoptosis induced by schizandrae-derived lignans in human leukemia HL-60 cells. |
| |
Authors: | Shigang Lin Makoto Fujii De-Xing Hou |
| |
Affiliation: | Department of Biochemical Science and Technology, Faculty of Agriculture, Kagoshima University, Korimoto 1-21-24, Kagoshima 890-0065, Japan. |
| |
Abstract: | Schizandrae chinensis, a traditional Chinese medicine herb, has been used to treat hepatitis B disease in Chinese hospital clinic. We have isolated two bioactive compounds, deoxyschizandrin and gamma-schizandrin, from S. chinensis. In the present, we reported that deoxyschizandrin and gamma-schizandrin could induce apoptosis in human promyelocytic leukemia cells (HL-60), as characterized by DNA fragmentation and poly (ADP) ribose polymerase (PARP) cleavage. Further molecular analysis showed that deoxyschizandrin and gamma-schizandrin caused the loss of mitochondrial membrane potential (DeltaPsim), cytochrome c release from mitochondrion to cytosol, truncation of Bid protein, and activation of caspase-3 and -9. However, they did not increase the intracellular level of reactive oxygen species (ROS). Antioxidants such as N-acetyl cysteine (NAC) and catalase did not block the apoptosis induced by deoxyschizandrin or gamma-schizandrin. These findings suggest that deoxyschizandrin and gamma-schizandrin-induced apoptosis in HL-60 cells involved ROS-independent mitochondrial dysfunction pathway. |
| |
Keywords: | Apaf-1, apoptotic protease-activating factor-1 DiOC6(3), 3,3′-dihexyloxacarbocyanine iodide H2DCF–DA, 2′,7′-dichlorofluorescein diacetate HL-60, human promyelocytic leukemia cells NAC, N-acetyl cysteine IC50, 50% inhibitory concentration PI, propidium iodide PARP, poly (ADP) ribose polymerase ROS, reactive oxygen species ΔΨm, mitochondrial membrane potential |
本文献已被 ScienceDirect 等数据库收录! |
|