Life SciencesCell BiologyPharmacologyApoptosisCell SignalingNeurotoxicologyApoptosis ModulationApoptosis RegulationApoptotic SignalingBcl-2 Family ProteinsCell DeathNeuronal Cell DeathBcl-2 Protein RegulationCaspase-mediated ApoptosisOxidative Stress - Induced ApoptosisOxidative Stress InjuryOxidative Stress-induced ApoptosisPro-apoptotic EffectorsProtective TreatmentsReactive Oxygen Species-induced Apoptosis
In this study, the effect of puerarin on hydrogen peroxide-induced apoptosis in PC12 cells was studied. Exposure of cells to 0.5mM 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.
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