PMID- 30108467
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20201001
IS  - 1611-2156 (Print)
IS  - 1611-2156 (Electronic)
IS  - 1611-2156 (Linking)
VI  - 17
DP  - 2018
TI  - Long-term administration of melatonin attenuates neuroinflammation in the aged 
      mouse brain.
PG  - 634-646
LID - 10.17179/excli2017-654 [doi]
AB  - Aging is often accompanied by a decline in cognitive function in conjunction with 
      a variety of neurobiological changes, including neuroinflammation. Melatonin is a 
      key endogenous indoleamine secreted by the pineal gland that plays a crucial role 
      in the regulation of circadian rhythms, is a potent free radical scavenger, has 
      anti-inflammatory activity and serves numerous other functions. However, the role 
      of melatonin in sterile inflammation in the brain has not been fully 
      investigated. In the present study, we investigated the neuroinflammation status 
      in aged mouse brains. The results showed that the protein levels of integrin alphaM 
      (CD11b), glial fibrillary acidic protein (GFAP), the major pro-inflammatory 
      cytokines (interleukin-1 beta [IL-1beta], interleukin-6 [IL-6], and tumor necrosis 
      factor alpha [TNF-alpha]) and phosphor-nuclear factor kappa B (pNFkappaB) were 
      significantly increased, while N-methyl-D-aspartate (NMDA) receptor subunits NR2A 
      and NR2B, Ca(2+)/calmodulin-dependent protein kinase II (CaMKII), and 
      brain-derived neurotrophic factor (BDNF) were down-regulated in the hippocampus 
      and prefrontal cortex (PFC) of 22-months-old (aged) mice compared with 
      2-months-old (young adult) mice. Melatonin was administered in the drinking water 
      to a cohort of the aged mice at a dose of 10 mg/kg/day, beginning at an age of 16 
      months for 6 months. Our results revealed that melatonin significantly attenuated 
      the alterations in these protein levels. The present study suggests an 
      advantageous role for melatonin in anti-inflammation, and this may lead to the 
      prevention of memory impairment in aging.
FAU - Permpoonputtana, Kannika
AU  - Permpoonputtana K
AD  - National Institute for Child and Family Development, Mahidol University, 
      Thailand.
FAU - Tangweerasing, Patlada
AU  - Tangweerasing P
AD  - Research Center for Neuroscience, Institute of Molecular Biosciences, Mahidol 
      University, Thailand.
FAU - Mukda, Sujira
AU  - Mukda S
AD  - Research Center for Neuroscience, Institute of Molecular Biosciences, Mahidol 
      University, Thailand.
FAU - Boontem, Parichart
AU  - Boontem P
AD  - Chulabhorn Graduate Institute, Chulabhorn Royal Academy, Thailand.
FAU - Nopparat, Chutikorn
AU  - Nopparat C
AD  - Research Center for Neuroscience, Institute of Molecular Biosciences, Mahidol 
      University, Thailand.
FAU - Govitrapong, Piyarat
AU  - Govitrapong P
AD  - Research Center for Neuroscience, Institute of Molecular Biosciences, Mahidol 
      University, Thailand.
AD  - Chulabhorn Graduate Institute, Chulabhorn Royal Academy, Thailand.
AD  - Department of Pharmacology, Faculty of Science, Mahidol University, Thailand.
LA  - eng
PT  - Journal Article
DEP - 20180702
PL  - Germany
TA  - EXCLI J
JT  - EXCLI journal
JID - 101299402
PMC - PMC6088215
OTO - NOTNLM
OT  - BDNF
OT  - NFkappaB
OT  - aging
OT  - melatonin
OT  - neuroinflammation
OT  - pro-inflammatory cytokine
EDAT- 2018/08/16 06:00
MHDA- 2018/08/16 06:01
PMCR- 2018/07/02
CRDT- 2018/08/16 06:00
PHST- 2017/07/21 00:00 [received]
PHST- 2018/06/11 00:00 [accepted]
PHST- 2018/08/16 06:00 [entrez]
PHST- 2018/08/16 06:00 [pubmed]
PHST- 2018/08/16 06:01 [medline]
PHST- 2018/07/02 00:00 [pmc-release]
AID - 2017-654 [pii]
AID - Doc634 [pii]
AID - 10.17179/excli2017-654 [doi]
PST - epublish
SO  - EXCLI J. 2018 Jul 2;17:634-646. doi: 10.17179/excli2017-654. eCollection 2018.