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

Mi Hyeon Jang, Sae Bin Jung, Myoung Hwa Lee, Chang Ju Kim, Young Taek Oh, Insug Kang, Jeongseon Kim, Ee Hwa Kim

Research output: Contribution to journalArticlepeer-review

71 Scopus citations


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 Aβ-induced cytotoxicity in microglial cells. Cells treated with Aβ exhibited several characteristic features of apoptosis, while cells pre-treated with melatonin prior to exposure to Aβ showed a decrease in the occurrence of such apoptotic features. Several previous studies have demonstrated the involvement of ROS in Aβ-induced neurotoxicity, and ROS generated by Aβ have been reported to lead to the activation of nuclear factor-kappa B (NF-κB), a transcription factor; pre-treatment with melatonin in the present study reduced the level of Aβ-induced intracellular ROS generation, inhibited NF-κB activation, and suppressed the Aβ-induced increase in caspase-3 enzyme activity. In addition, it was found that pre-treatment with melatonin inhibits Aβ-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 Aβ-induced apoptosis.

Original languageEnglish (US)
Pages (from-to)26-31
Number of pages6
JournalNeuroscience Letters
Issue number1-2
StatePublished - May 20 2005


  • Amyloid β
  • Apoptosis
  • Caspase-3
  • Melatonin
  • Nuclear factor-kappa B
  • Reactive oxygen species

ASJC Scopus subject areas

  • General Neuroscience


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