Granulocyte Colony-stimulating Factor Attenuates Chronic Neuroinflammation in the Brain of Amyloid Precursor Protein Transgenic Mice: an Alzheimer’s Disease Mouse Model  

Oleh:

Jiang, H ; LIU, CX ; FENG, JB

Jenis: Article from Journal - ilmiah internasional
Dalam koleksi: The Journal of International Medical Research vol. 38 no. 04 (Jul. 2010), page 1305-1312.
Topik: granulocyte colony-stimulating factor; inflammation; alzheimer's disease; amyloid precursor protein; nicotinic acetylcholine receptor

Ketersediaan

Perpustakaan FK Nomor Panggil: J11.K.2010.02 Non-tandon: 1 (dapat dipinjam: 0) Tandon: tidak ada

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Isi artikel

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 alpha7 nicotinic acetylcholine receptor (alpha7 nAChR) pathway. Mice transgenic for the V171I mutant amyloid precursor protein (APP) were injected subcutaneously with G-CSF 50 micro-g/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 alpha7 nAChR protein were significantly increased and levels of interleukin-1beta, tumour necrosis factor-alpha and nuclear factor-kappaB (NF-kappaB) protein were significantly decreased in the brain of APP transgenic mice in response to G-CSF. Levels of alpha7 nAChR protein correlated negatively with NF-kappaB levels. It is concluded that G-CSF might attenuate inflammation by down-regulating NF-kappaB and up-regulating alpha7 nAChR in the brain of APP transgenic mice, indicating a potential new therapeutic approach to Alzheimer’s disease.

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