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Atorvastatin attenuates the production of IL-1β, IL-6, and TNF-α in the hippocampus of an amyloid β1-42-induced rat model of Alzheimer’s disease

Authors Zhang YY, Fan YC, Wang M, Wang D, Li XH

Received 16 November 2012

Accepted for publication 20 December 2012

Published 31 January 2013 Volume 2013:8 Pages 103—110


Checked for plagiarism Yes

Review by Single anonymous peer review

Peer reviewer comments 3

Yuan-Yuan Zhang,1,2* Yu-Chen Fan,3* Min Wang,1,2 Dong Wang,1,2 Xiao-Hong Li1,2

1Department of Neurology, Jinan Central Hospital affiliated to Shandong University, Jinan, People’s Republic of China; 2School of Medicine, Shandong University, Jinan, People’s Republic of China; 3Department of Hepatology, Qilu Hospital of Shandong University, Jinan, People’s Republic of China

*Yuan-Yuan Zhang and Yu-Chen Fan contributed equally to this work

Background and aim: Amyloid-beta (Aβ) peptide is reported to initiate flexible inflammation in the hippocampus of the human brain in Alzheimer’s disease (AD). The present study aimed to investigate the possible effects of atorvastatin on the production of inflammation cytokines in the hippocampus and the potential impacts on behavioral ability, in an AD model.
Methods: We firstly established AD rat models using intracerebroventricular injection of Aβ1-42. A Morris water maze was also performed to determine the spatial learning and memory ability in the AD models. Intracellular staining of interleukin (IL)-1β, IL-6, and tumor necrosis factor alpha was determined using immunohistochemical staining at 6 hours and day 7 after the injection of Aβ.
Results: The escape latency of the atorvastatin-treated AD group (5 mg/kg/d) was significantly shorter than that of AD group on day 3 (41 ± 1.05 seconds versus 47 ± 1.05 seconds, P < 0.01) and day 4 (34 ± 1.25 seconds versus 43 ± 1.01 seconds, P < 0.01) after the beginning of the training. Furthermore, the atorvastatin-treated AD group displayed a significant higher mean number of annulus crossings than did the AD group (2.9 ± 0.5 versus 2.4 ± 0.9, P < 0.05). Fewer injured nerve cells and proliferated glial cells were also demonstrated in the atorvastatin-treated AD group than in the AD group. Of great importance, we demonstrated that IL-1β, IL-6, and tumor necrosis factor alpha were significantly decreased in the atorvastatin-treated AD group than that in the AD group.
Conclusion: Atorvastatin might attenuate the damage of nerve cells and improve learning and memory ability by inhibiting inflammatory response in the progression of AD.

Keywords: amyloid-beta, inflammation, interleukin-1β, interleukin-6, tumor necrosis factor

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