Melatonin attenuates amyloid beta25-35-induced apoptosis in mouse microglial BV2 cells

Melatonin has been reported to possess strong antioxidant actions, and is able to directly scavenge a variety of reactive oxygen species (ROS). The present study investigated whether melatonin possesses protective effects against A beta-induced cytotoxicity in microglial cells. Cells treated with A beta exhibited several characteristic features of apoptosis, while cells pre-treated with melatonin prior to exposure to A beta showed a decrease in the occurrence of such apoptotic, features. Several previous studies have demonstrated the involvement of ROS in A beta-induced neurotoxicity, and ROS generated by A beta have been reported to lead to the activation of nuclear factor-kappa B (NF-kappa B), a transcription factor; pre-treatment with melatonin in the present study reduced the level of A beta-induced intracellular ROS generation, inhibited NF-kappa B activation, and suppressed the A beta-induced increase in caspase-3 enzyme activity. In addition, it was found that pre-treatment with melatonin inhibits A beta-induced increase in the levels of bax mRNA and that it enhances the level of bcl-2 expression. Based on these findings, the authors speculate that melatonin may provide an effective means of treatment for Alzheimer's disease through attenuation of A beta-induced apoptosis. (c) 2005 Elsevier Ireland Ltd. All rights reserved.