Effects of baicalin against oxidative stress injury of SH-SY5Y cells by up-regulating SIRT1.
- Author:
Hong-yan CHEN
1
;
Miao GENG
;
Ya-zhuo HU
;
Jian-hua WANG
Author Information
1. Institute of Geriatrics, Chinese PLA General Hospital, Beijing 100853, China.
- Publication Type:Journal Article
- MeSH:
Antioxidants;
isolation & purification;
pharmacology;
Apoptosis;
drug effects;
Caspase 3;
metabolism;
Cell Line, Tumor;
Cell Survival;
drug effects;
Flavonoids;
isolation & purification;
pharmacology;
Humans;
Hydrogen Peroxide;
toxicity;
L-Lactate Dehydrogenase;
metabolism;
Neuroblastoma;
metabolism;
pathology;
Nitric Oxide;
metabolism;
Oxidative Stress;
drug effects;
Plants, Medicinal;
chemistry;
Scutellaria;
chemistry;
Sirtuin 1;
metabolism;
Up-Regulation
- From:
Acta Pharmaceutica Sinica
2011;46(9):1039-1044
- CountryChina
- Language:Chinese
-
Abstract:
This study is to investigate the effect of baicalin (BL) against oxidative injury stress of SH-SY5Y cells induced by H2O2 and the possible mechanism. SH-SY5Y cells were pre-incubated with baicalin (25, 50, and 100 micromol x L(-1)) for 12 h prior to exposure to H2O2 (150 micromol x L(-1)) for 24 h. The viability of SH-SY5Y cells was measured by MTT assay. The contents of LDH and NO were determined. The percentage of apoptotic cells was assessed by flow cytometry (FCM). The content of Caspase-3 was tested by immunofluorescence histochemical method. BL at 50 and 100 micromol x L(-1) separately increased the cell viability and up-regulated SIRT1, reduced the contents of LDH, NO, Caspase-3 and the apoptotic percentage of SH-SY5Y cells. This study results suggest that baicalin could inhibit the H2O2-induced neuronal apoptosis. The further mechanism studies show that baicalin inhibit apoptosis via reducing Caspase-3 expression and up-regulating SIRT1.
