Long-term administration of melatonin attenuates neuroinflammation in the aged mouse brain
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Date
2018-07-02
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Abstract
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 αM (CD11b), glial fibrillary acidic protein
(GFAP), the major pro-inflammatory cytokines (interleukin-1 beta [IL-1β], interleukin-6 [IL-6], and tumor necrosis
factor alpha [TNF-α]) and phosphor-nuclear factor kappa B (pNFκB) were significantly increased, while Nmethyl-
D-aspartate (NMDA) receptor subunits NR2A and NR2B, Ca2+/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.
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Keywords
Aging, Neuroinflammation, Melatonin, Pro-inflammatory cytokine, NFkB, BDNF