Protective effect of baicalin against rotenone induced injury on PC12 cells.
- Author:
Hai-Lie JI
;
Li-Guo TONG
;
Chong-Zhi BAI
;
Mei-Qing SONG
;
Nai-Hong CHEN
;
Ma-Li FENG
- Publication Type:Journal Article
- MeSH: Animals; Apoptosis; drug effects; Caspase 3; metabolism; Cell Survival; drug effects; Cytoprotection; drug effects; Flavonoids; pharmacology; Gene Expression Regulation; drug effects; Intracellular Space; drug effects; metabolism; PC12 Cells; Proto-Oncogene Proteins c-bcl-2; metabolism; Rats; Reactive Oxygen Species; metabolism; Rotenone; pharmacology; bcl-2-Associated X Protein; metabolism
- From: China Journal of Chinese Materia Medica 2014;39(15):2947-2951
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo explore the protective effect of baicalin against rotenone-induced injury on PC12 cells, and the po-tential mechanism of action action was also explored.
METHODPC12 cells were injured by rotenone and were treated with different concentrations (0.1, 1, 10 μmol x L(-1)) of baicalin at the same time. Cell viability was analyzed by MTT, and morphology was observed by phase-contrast microscopy. The cell apoptosis was detected by flow cytometry by Annexin V-FITC/PI staining. The intracellular ROS level was determined by fluorescence microscope with DCF-DA staining. The expression of Bcl-2, Bax and Caspase-3 was analyzed by Western blot.
RESULTThe viability of PC12 cells exposure to rotenone for 24 hour was gradually decreased with dose escalating and 1.5 μmol x L was adopted to do the following experiment. Baicalin increased cell viability, improved cell morphology and decreased intracellular ROS level. Moreover, FACS indicated baicalin attenuated the apoptosis induced by rotenone significantly. Western blot showed that Bcl-2, Bax and Caspase-3 expression in rotenone-induced PC12 cells was reversed by baicalin.
CONCLUSIONThis study has demonstrated that baicalin protects PC12 cells against rotenone-induced apoptosis, at least in part, by scavenging excessive ROS and inhibiting the mitochondrion-dependent apoptotic pathway.