摘要
Oxidative stress has been implicated to play a crucial role in the pathogenesis of Alzheimer’s disease (AD). Currently, it is known that numerous signaling pathways involved in neurodegenerative disorders are activated in response to oxidative stress. Recent directions on AD treatments have focused on the use of antioxidants including Curcumin, a hydrophobic polyphenol derived from the rhizome of the herb Curcuma longa, to augment the intracellular antioxidant defences. In the present study, hydrogen peroxide (H2O2) was used to evaluate the effects of oxidative stress on apoptotic SK-N-MC cells death with focus on changes in activity of Notch signaling pathway. The extent of lipid peroxidation, protein oxidation and intracellular ROS (Reactive Oxygen Species) levels was investigated as oxidative stress biomarkers. Here, we showed that H2O2 reduced GSH levels and activity of antioxidant enzymes and also influenced Notch signaling activation. The present data concluded that Curcumin protected cells against oxidative stress-induced apoptosis.
Oxidative stress has been implicated to play a crucial role in the pathogenesis of Alzheimer’s disease (AD). Currently, it is known that numerous signaling pathways involved in neurodegenerative disorders are activated in response to oxidative stress. Recent directions on AD treatments have focused on the use of antioxidants including Curcumin, a hydrophobic polyphenol derived from the rhizome of the herb Curcuma longa, to augment the intracellular antioxidant defences. In the present study, hydrogen peroxide (H2O2) was used to evaluate the effects of oxidative stress on apoptotic SK-N-MC cells death with focus on changes in activity of Notch signaling pathway. The extent of lipid peroxidation, protein oxidation and intracellular ROS (Reactive Oxygen Species) levels was investigated as oxidative stress biomarkers. Here, we showed that H2O2 reduced GSH levels and activity of antioxidant enzymes and also influenced Notch signaling activation. The present data concluded that Curcumin protected cells against oxidative stress-induced apoptosis.
