Abstract: Objective   To explore changes of pro- and anti-inflammatory cytokines expression in the hippocampus of Aβ1-42- induced AD rat model. Methods   Sprague Dawley rats (200 ± 20 g) were injected Aβ1-42 , the escape latency was evaluated by Morris water maze. Lesion of neurons within the hippocampus CA1 area was detected by Nissl staining. The levels of amyloid precursor protein (APP) and protein phosphatase 2A (PP2A) in hippocampus were measured by means of Western blot analyses. Real-time PCR was employed to examine the expressions of pro- inflammatory cytokines, including interleukin-1β (IL-1β), tumor necrosis factor-α (TNF-α), interferon-γ (IFN-γ), and anti-inflammatory cytokines including IL-4, IL-10, transforming growth factor-β (TGF-β). Results   Rats subjected to Aβ1-42 injection within bilateral hippocampus confirmed the success to make AD rat models, which led to reduction of the ability of learning and memory; Nissl staining showed pyramidal cells disturbed, neurons decreased significantly. the treatment with Aβ1-42 notably increased expression of APP but decreased PP2A expression level. There was evidently up-regulation in the expressions of pro-inflammatory mediator mRNAs in AD rats, including IL-1β, TNF-α and IFN-γ. Contrarily, the expressions of anti-inflammatory cytokine mRNAs, including IL-4, IL-10 and TGF-β, were significantly down-regulated relative to the control rats. Conclusions   Aβ1-42 injection in bilateral rat hippocampus induces AD model. Neuroinflammation resulting from pro- and anti-inflammatory unbalance is involved in pathogenesis of AD.

Key words: Alzheimer's disease, hippocampus, amyloid beta-protein, amyloid beta-protein precursor, protein phosphatase 2, cytokines, cytokines, SpragueDawley