Effect of Scutellaria barbata extract against human hepatocellular Hep-G2 cell proliferation and its mechanism.
- Author:
Jing-ming LIN
1
;
Yu LIU
;
Rong-cheng LUO
Author Information
- Publication Type:Journal Article
- MeSH: Antineoplastic Agents, Phytogenic; pharmacology; Apoptosis; drug effects; Carcinoma, Hepatocellular; pathology; physiopathology; ultrastructure; Cell Cycle; drug effects; Cell Line, Tumor; Cell Proliferation; drug effects; Dose-Response Relationship, Drug; Drugs, Chinese Herbal; pharmacology; Flow Cytometry; Humans; Liver Neoplasms; pathology; physiopathology; ultrastructure; Microscopy, Electron, Transmission; Plant Extracts; pharmacology; Proto-Oncogene Proteins c-bcl-2; analysis; Scutellaria; chemistry; bcl-2-Associated X Protein; analysis; fas Receptor; analysis
- From: Journal of Southern Medical University 2006;26(7):975-977
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo observe the effects of Scutellaria barbata extract (ESB) on human hepatoma cell line Hep-G2 proliferation in vitro and explore the mechanism.
METHODSThe inhibitory effect of ESB on Hep-G2 proliferation was estimated by MTT assay, and the morphological changes of the cells were observed under optical and electron microscopes. Distribution of cell cycle, cell apoptosis and the protein expressions of apoptosis-associated genes as bcl-2, bax and fas were analyzed using flow cytometry.
RESULTSESB inhibited the proliferation of Hep-G2 cells in a time- and dose-dependent manner. ESB treatment for 72 h resulted in changes of early apoptotic morphology of the cells as observed under optical and the transmission electron microscopes and increased cell apoptosis. Cell cycle analysis revealed decreased S-phase and increased G0/G1-phase cells. Fas expression was significantly up-regulated in response to ESB treatment whereas Bcl-2 and Bax expressions underwent no significant changes.
CONCLUSIONESB can inhibit Hep-G2 cell proliferation, induce cell cycle block, and increase cell apoptosis, which may relate to the activation of FNFR superfamily.
