Effect of (m)VD-hemopressin against Aβ1-42-induced oxidative stress and apoptosis in mouse hippocampal neurons

This study aimed to clarify the mechanism by which VD protects hippocampal neurons against Aβ1-42-induced impairment. Our results showed that VD inhibited oxidative stress injury induced by Aβ1-42, as demonstrated by the VD-induced reversal of the upregulation of reactive oxygen species (ROS) and the intracellular lipid peroxidation product malondialdehyde (MDA) and the downregulation of the activities of the antioxidative enzymes catalase (CAT) and glutathione peroxidase (GSH-PX) in mouse hippocampal neurons. We also found that VD restored the decrease in cell growth and viability induced by Aβ1-42 and reversed Aβ1-42-induced apoptosis mediated by the apoptosis-associated proteins Bcl-2 and Bax. However, cotreatment with AM251 (an antagonist of CB1R) blocked the effects of VD. In brief, this study suggested that through CB1R, VD reversed the impairment of cell growth and viability, oxidative stress injury and apoptosis induced by Aβ1-42. Therefore, VD may be a promising agent for the treatment of diseases that involve oxidative stress injury and apoptosis induced by Aβ1-42, such as AD.

Source: Peptides - November 13, 2019 Category: Biochemistry Source Type: research