Mei Hanfang,Li He,Zhu Jiayong.Cell cycle regulation involved in protective effect of proanthocyanidins on PC12 cells damage from hydrogen peroxide[J].J Amry Med Univ (J Third Mil Med Univ),2014,36(17):1809-1812.
Mei Hanfang,Li He,Zhu Jiayong.Cell cycle regulation involved in protective effect of proanthocyanidins on PC12 cells damage from hydrogen peroxide[J].J Amry Med Univ (J Third Mil Med Univ),2014,36(17):1809-1812.DOI:
Cell cycle regulation involved in protective effect of proanthocyanidins on PC12 cells damage from hydrogen peroxide
Objective To determine the protective effect of proanthocyanidins on oxidative damage and cell cycle arresting in PC12 cells induced by hydrogen peroxide
and to investigate the role of cell cycle regulatory genes cellular-Abelson gene (c-Abl) and polo-like kinase-1 (plk1) in the protection. Methods PC12 cells were incubated with different concentrations of proanthocyanidins and induced by 100 μmol/L hydrogen peroxide for 6 h
and then the cell viability was measured by MTT assay
and the distribution of cell cycle was measured by flow cytometry
and the protein expression of c-Abl and plk1 was detected by Western blotting. Results Compared with the PC12 cells in control group
hydrogen peroxide significantly decreased cell viability and increased S phase distribution in PC12 cells (P0.01)
and the protein expression level of c-Abl and plk1 gene in PC12 cells was also increased significantly by hydrogen peroxide (P0.01); Compared with the group of PC12 cells induced by hydrogen peroxide
proanthocyanidins significantly increased cell viability of PC12 cells in the range of experimental doses (P0.01). Proanthocyanidins relieved the S phase arrest induced by hydrogen peroxide (P0.01)
and the protein levels of c-Abl and plk1 in PC12 cells was also decreased by proanthocyanidins in a dose- dependent manner (P0.01). Conclusion Proanthocyanidins can protect PC12 cells from the cytotoxic stresses induced by hydrogen peroxide
and the protective mechanism may be mediated by relieving the S phase arrest and decreasing the protein expressional level of c-Abl and plk1 gene.