Granulocyte colony-stimulating factor attenuates chronic neuroinflammation in the brain of amyloid precursor protein transgenic mice: an Alzheimer's disease mouse model.
J Int Med Res
; 38(4): 1305-12, 2010.
Article
em En
| MEDLINE
| ID: mdl-20926003
ABSTRACT
Recent evidence suggests that inflammatory mechanisms contribute significantly to the progression of Alzheimer's disease. Granulocyte colony-stimulating factor (G-CSF) is an anti-inflammatory immunomodulator, but the mechanism of its anti-inflammatory effect is unclear. This study was designed to investigate whether G-CSF could inhibit inflammation in a mouse model of Alzheimer's disease through an α7 nicotinic acetylcholine receptor (α7 nAChR) pathway. Mice transgenic for the V171I mutant amyloid precursor protein (APP) were injected subcutaneously with G-CSF 50 µg/kg per day or phosphate-buffered saline (PBS; control group) for 7 days, and wild-type C57/BL6 mice were injected with PBS daily for 7 days. Mice were killed on days 7, 14 and 28 after treatment began. Levels of α7 nAChR protein were significantly increased and levels of interleukin-1ß, tumour necrosis factor-α and nuclear factor-κB (NF-κB) protein were significantly decreased in the brain of APP transgenic mice in response to G-CSF. Levels of α7 nAChR protein correlated negatively with NF-κB levels. It is concluded that G-CSF might attenuate inflammation by down-regulating NF-κB and up-regulating α7 nAChR in the brain of APP transgenic mice, indicating a potential new therapeutic approach to Alzheimer's disease.
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Base de dados:
MEDLINE
Assunto principal:
Encéfalo
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Fator Estimulador de Colônias de Granulócitos
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Precursor de Proteína beta-Amiloide
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Doença de Alzheimer
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Inflamação
Idioma:
En
Ano de publicação:
2010
Tipo de documento:
Article