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

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

Research output: Contribution to journalArticle

67 Citations (Scopus)

Abstract

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
Volume380
Issue number1-2
DOIs
StatePublished - May 20 2005
Externally publishedYes

Fingerprint

Melatonin
Amyloid
Apoptosis
Reactive Oxygen Species
NF-kappa B
Caspase 3
Alzheimer Disease
Transcription Factors
Antioxidants
Messenger RNA
Enzymes

Keywords

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

ASJC Scopus subject areas

  • Neuroscience(all)

Cite this

Melatonin attenuates amyloid beta25-35-induced apoptosis in mouse microglial BV2 cells. / Jang, Mi-Hyeon D; Jung, Sae Bin; Lee, Myoung Hwa; Kim, Chang Ju; Oh, Young Taek; Kang, Insug; Kim, Jeongseon; Kim, Ee Hwa.

In: Neuroscience Letters, Vol. 380, No. 1-2, 20.05.2005, p. 26-31.

Research output: Contribution to journalArticle

Jang, Mi-Hyeon D ; Jung, Sae Bin ; Lee, Myoung Hwa ; Kim, Chang Ju ; Oh, Young Taek ; Kang, Insug ; Kim, Jeongseon ; Kim, Ee Hwa. / Melatonin attenuates amyloid beta25-35-induced apoptosis in mouse microglial BV2 cells. In: Neuroscience Letters. 2005 ; Vol. 380, No. 1-2. pp. 26-31.
@article{a3134c3399dd4605922800daddf47622,
title = "Melatonin attenuates amyloid beta25-35-induced apoptosis in mouse microglial BV2 cells",
abstract = "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.",
keywords = "Amyloid β, Apoptosis, Caspase-3, Melatonin, Nuclear factor-kappa B, Reactive oxygen species",
author = "Jang, {Mi-Hyeon D} and Jung, {Sae Bin} and Lee, {Myoung Hwa} and Kim, {Chang Ju} and Oh, {Young Taek} and Insug Kang and Jeongseon Kim and Kim, {Ee Hwa}",
year = "2005",
month = "5",
day = "20",
doi = "10.1016/j.neulet.2005.01.003",
language = "English (US)",
volume = "380",
pages = "26--31",
journal = "Neuroscience Letters",
issn = "0304-3940",
publisher = "Elsevier Ireland Ltd",
number = "1-2",

}

TY - JOUR

T1 - Melatonin attenuates amyloid beta25-35-induced apoptosis in mouse microglial BV2 cells

AU - Jang, Mi-Hyeon D

AU - Jung, Sae Bin

AU - Lee, Myoung Hwa

AU - Kim, Chang Ju

AU - Oh, Young Taek

AU - Kang, Insug

AU - Kim, Jeongseon

AU - Kim, Ee Hwa

PY - 2005/5/20

Y1 - 2005/5/20

N2 - 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.

AB - 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.

KW - Amyloid β

KW - Apoptosis

KW - Caspase-3

KW - Melatonin

KW - Nuclear factor-kappa B

KW - Reactive oxygen species

UR - http://www.scopus.com/inward/record.url?scp=18044386381&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=18044386381&partnerID=8YFLogxK

U2 - 10.1016/j.neulet.2005.01.003

DO - 10.1016/j.neulet.2005.01.003

M3 - Article

C2 - 15854745

AN - SCOPUS:18044386381

VL - 380

SP - 26

EP - 31

JO - Neuroscience Letters

JF - Neuroscience Letters

SN - 0304-3940

IS - 1-2

ER -