Changes of Cytokine Expression in the Hippocampus of Aβ1-42-Induced Alzheimer’s Disease Rat Model
10.3969/j.issn.0253-9896.2013.08.040
- VernacularTitle:Aβ1-42诱导阿尔茨海默病模型大鼠海马内细胞因子表达变化的研究*
- Author:
Xuemei ZHANG
;
Kaifu KE
;
Xiaoxia FANG
;
Yihua QIU
;
Yuping PENG
- Publication Type:Journal Article
- Keywords:
alzheimer disease;
hippocampus;
amyloid beta-protein;
amyloid beta-protein precursor;
protein phos-phatase 2;
cytokines;
rats,Sprague-Dawley
- From:
Tianjin Medical Journal
2013;(8):789-792
- CountryChina
- Language:Chinese
-
Abstract:
Objective To explore changes of expression of pro-and anti-inflammatory cytokines in the hippocam-pus of Aβ1-42-induced Alzheimer’s disease (AD) rat model. Methods Twenty-four SD rats were divided into control group, PBS group (PBS was injected into CA1 area of hippocampus) and AD model group (Aβ1-42 was injected into CA1 area of hip-pocampus). The escape latency was evaluated by Morris water maze in three groups. Nissl staining was used to detect the le-sions of hippocampal CA1 neurons. Levels of amyloid precursor protein (APP) and protein phosphatase 2A (PP2A) in hippo-campus were measured by Western blot analysis. Real-time PCR was employed to examine the expressions of pro-inflamma-tory cytokines, including interleukin-1β (IL-1β), tumor necrosis factor-α (TNF-α) and interferon-γ (IFN-γ), and the mRNA expressions of anti-inflammatory cytokines, including IL-4, IL-10 and transforming growth factor-β(TGF-β). Re-sults Rats subjected to Aβ1-42 injection in bilateral hippocampus led to a ability reduction of learning and memory, a loss of neurons in hippocampus and an increase in the expression of APP, and a decrease in PP2A expression in the hippocampus. In AD hippocampus, The mRNA expressions of the pro-inflammatory mediator, IL-1β, TNF-αand IFN-γ, were significant-ly up-regulated, but the expressions of the anti-inflammatory cytokines, IL-4, IL-10 and TGF-β, were markedly down-reg-ulated in AD group compared with those of control and PBS groups. Conclusion The pro-inflammatory/anti-inflammatory imbalance induced neuro-inflammation in AD rats, which was involved in pathogenesis of AD.
