Study on p38MAPK pathway in HepG-2 cells apoptosis induced by sulforaphane
Sun Sheng-nan
Abstract
Sun Sheng-nan
Abstract
Objective: To investigate the roles of p38 mitogen/activated protein kinase in the apoptosis induced by sulforaphane(SFN) in HepG-2 cells. Methods: Annexin V-FITC staining was used to observe the morphology of apoptotic cells treated with different dosages of SFN for 48 h. Western Blotting was employed to detect the expression of p38 and p-p38 proteins. Results: SFN could obviously induce the cell apoptosis of HepG-2 cells and the apoptotic rate after treated with SFN at the dosage of 10, 20, and 40 μmol/L was 27.42 %, 46.53 %, and 58.92 %, respectively. Western Blotting pointed that the expression of p-p38 proteins was evidently reduced by SFN(P 0.05), meanwhile, there was no remarkable change on the expression of p38 protein. Conclusion: SFN could induce the cell apoptosis of HepG-2 cells by interdicting p38MAPK pathway in HepG-2 cells.
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Objective: To investigate the roles of p38 mitogen/activated protein kinase in the apoptosis induced by sulforaphane(SFN) in HepG-2 cells. Methods: Annexin V-FITC staining was used to observe the morphology of apoptotic cells treated with different dosages of SFN for 48 h. Western Blotting was employed to detect the expression of p38 and p-p38 proteins. Results: SFN could obviously induce the cell apoptosis of HepG-2 cells and the apoptotic rate after treated with SFN at the dosage of 10, 20, and 40 μmol/L was 27.42 %, 46.53 %, and 58.92 %, respectively. Western Blotting pointed that the expression of p-p38 proteins was evidently reduced by SFN(P 0.05), meanwhile, there was no remarkable change on the expression of p38 protein. Conclusion: SFN could induce the cell apoptosis of HepG-2 cells by interdicting p38MAPK pathway in HepG-2 cells.
Key concepts: Apoptosis, Annexin, Blot, p38 mitogen-activated protein kinases, Sulforaphane, Chemistry, Molecular biology, Cell