Study on norcantharidin-induced apoptosis in SMMC-7721 cells through mitochondrial pathways.
- Author:
Xian-qian LI
1
;
Shi-he SHAO
;
Gui-lian FU
;
Xiao-hong HAN
;
Hong GAO
Author Information
- Publication Type:Journal Article
- MeSH: Apoptosis; drug effects; Apoptosis Inducing Factor; metabolism; Blotting, Western; Bridged Bicyclo Compounds, Heterocyclic; pharmacology; Caspase 3; metabolism; Cell Line, Tumor; Cytochromes c; metabolism; Flow Cytometry; Humans; Liver Neoplasms; enzymology; metabolism; pathology; Membrane Potentials; drug effects; Mitochondria; drug effects; metabolism; bcl-2-Associated X Protein; metabolism
- From: Chinese journal of integrative medicine 2010;16(5):448-452
- CountryChina
- Language:English
-
Abstract:
OBJECTIVETo investigate the mechanism of norcantharidin (NCTD)-induced SMMC-7721 hepatoma cell apoptosis.
METHODSSMMC-7721 cell growth inhibition was measured by the MTT method. Apoptosis was detected by Annexin V/propidium iodide staining. The mitochondrial membrane potential was measured by flow cytometry. Western blot analysis was used to evaluate the level of cytochrome c, caspase-3, AIF, Bcl-2 and Bax expression.
RESULTSNCTD inhibited SMMC-7721 cell growth in a time- and dose-dependent manner. The cells treated with NCTD showed the loss of mitochondrial membrane potential. The activities of caspase-3, cytochrome c, AIF, and Bax were up-regulated after NCTD treatment at different doses. The expression of Bcl-2 was decreased after treatment with NCTD.
CONCLUSIONSNCTD could induce SMMC-7721 cell apoptosis. The activation of the mitochondrial pathway was involved in the process of NCTD-induced SMMC-7721 cell apoptosis.
