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Hydrogen peroxide‐induced apoptosis in pc12 cells and the protective effect of puerarin
Author(s) -
Jiang B.,
Liu J. H.,
Bao Y. M.,
An L. J.
Publication year - 2003
Publication title -
cell biology international
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.932
H-Index - 77
eISSN - 1095-8355
pISSN - 1065-6995
DOI - 10.1016/j.cellbi.2003.09.007
Subject(s) - puerarin , apoptosis , hydrogen peroxide , chemistry , microbiology and biotechnology , caspase 3 , downregulation and upregulation , oxidative stress , biology , programmed cell death , biochemistry , medicine , gene , alternative medicine , pathology
In this study, the effect of puerarin on hydrogen peroxide‐induced apoptosis in PC12 cells was studied. Exposure of cells to 0.5 mM H 2 O 2 may cause significant viability loss and apoptotic rate increase. When c‐Myc, Bcl‐2 and Bax expression and caspase‐3 activity were measured, using Ac‐DEVD‐AMC as a substrate, the changes in these apoptosis regulatory and effector proteins suggested that the elevation of c‐Myc, decrease in Bcl‐2: Bax protein ratio, and caspase‐3 activation all play a key role in apoptosis. When cells were treated with puerarin prior to 0.5 mM H 2 O 2 treatment, a reduction in viability loss and apoptotic rate was seen. In addition, c‐Myc expression decreased and Bcl‐2: Bax ratio increased. Puerarin also reduced the H 2 O 2 ‐induced elevation of caspase‐3 activation. These results suggest that puerarin can protect neurons against oxidative stress. It can block apoptosis in its early stages via the regulation of anti‐ and pro‐apoptotic proteins, as well as by the attenuation of caspase‐3 activation in H 2 O 2 ‐induced PC12 cells.