Effect of melatonin on glial fibrillary acidic protein, nuclear factor-kB and synaptophysin expressions in aging mice.
- Author:
Li ZHOU
1
;
Qing-ren ZENG
;
Jun ZHOU
Author Information
- Publication Type:Journal Article
- MeSH: Aging; metabolism; Animals; Brain; metabolism; Chimera; Glial Fibrillary Acidic Protein; Male; Melatonin; pharmacology; Mice; Mice, Inbred C3H; Mice, Inbred C57BL; NF-kappa B; genetics; metabolism; Nerve Tissue Proteins; genetics; metabolism; Synaptophysin; genetics; metabolism; Transcription Factor RelA; genetics; metabolism
- From: Journal of Southern Medical University 2011;31(12):2043-2047
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo study the effect of melatonin on the expressions of glial fibrillary acidic protein (GFAP), nuclear factor-κB (NF-κB p65) and synaptophysin in mice of different ages.
METHODSTwenty young male B6C3F1 mice (5.5 months) and 20 aged mice (26 months) were both divided into control and melatonin treatment (daily dose of 0.04 mg/kg) groups. After 2.5 months of treatment, the brain tissues of the mice were collected to examine the expressions of GFAP, NF-κB and SYN by immunohistochemistry.
RESULTSIn the control groups, the expression of NF-κB p65 in the brain tissue increased with age, whereas a reverse change was found in melatonin-treated aged rats (P<0.05). Synaptophysin expression also decreased with age, but melatonin treatment significantly enhanced its expression in aged mice (P<0.05). GFAP expression in the brain tissue increased with age regardless of melatonin treatment (P>0.05).
CONCLUSIONGFAP expression is almost not affected by melatonin treatment in aged mice. Melatonin can reduce the expression levels of NF-κB p65 and synaptophysin in the brain tissue to protect the brain and slow down the aging process.