Antagonism of baicalin on cell cyclical distribution and cell apoptosis in A549 cells infected with influenza A (H1N1) virus.
- Author:
Chun-jing ZHANG
1
;
Li-gang GU
;
Hai-tao YU
Author Information
1. Department of Biochemistry and Molecular Biology, Qiqihar Medical College, Qiqihar 161042, China. cjzhang2005@yahoo.com.cn
- Publication Type:Journal Article
- MeSH:
Antiviral Agents;
pharmacology;
Apoptosis;
drug effects;
Caspases;
metabolism;
Cell Cycle;
drug effects;
Cell Line, Tumor;
Flavonoids;
pharmacology;
Flow Cytometry;
Humans;
Influenza A Virus, H1N1 Subtype;
drug effects;
physiology
- From:
Chinese Journal of Virology
2011;27(2):108-116
- CountryChina
- Language:Chinese
-
Abstract:
To observe the inhibitive effect of Baicalin against influenza A H1N1 virus infection in epithelial cell line A549, the cell proliferation and cytotoxicity were assayed by MTT, the cell cycle and the apoptosis were analyzed by flowcytometer using PI staining, the morphology of cellular nucleolus was observed by Hoechst 33258 staining and the effects of activation on caspase 3 and caspase 8/9 were also detected by immunofluorescent staining with a fluorescence microscope. The results showed that Baicalin exerted an inhibitive effect on CPE after influenza A H1N1 virus infection. The FACS with PI staining showed that the cell cycle of the infected cell was arrested at S phase, the Baicalin-treated group decreased S phase cell ratio and subG0 phase peak in comparison with the control (P < 0.05) and significantly promoted cell proliferation (# P < 0.05). Hoechst33258 staining suggested that Baicalin protected the cellular nucleolus against the influenza virus-induced apoptosis. Observation under the immunofluorescent microscope suggested that the activities of caspase-8 and caspase-3 were enhanced at 36 h post the influenza virus infection, but 100 microg/mL Baicalin suppressing the activation of caspase-8 and caspase-3 rather than that of caspase-9. In summary, this research confirmed that Baicalin inhibited the influenza A H1N1 virus strain infection in vitro, the drug obviously protected cells from apoptosis damages through regulating cell cycle and suppressed the activation of caspase-8 and caspase-3. The down-regulation was significant and showed a dose-dependent relationship.
