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Atorvastatin prevents amyloid-β peptide oligomer-induced synaptotoxicity and memory dysfunction in rats through a p38 MAPK-dependent pathway

  
@article{APS5941,
	author = {Ling-ling Zhang and Hai-juan Sui and Bing Liang and Han-ming Wang and Wen-hui Qu and Sheng-xue Yu and Ying Jin},
	title = {Atorvastatin prevents amyloid-β peptide oligomer-induced synaptotoxicity and memory dysfunction in rats through a p38 MAPK-dependent pathway},
	journal = {Acta Pharmacologica Sinica},
	volume = {35},
	number = {6},
	year = {2016},
	keywords = {},
	abstract = {Ling-ling ZHANG, Hai-juan SUI, Bing LIANG, Han-ming WANG, Wen-hui QU, Sheng-xue YU, Ying JIN*
Department of Pharmacology, Liaoning Medical University, Jinzhou 121001, China
 
Aim: To investigate whether atorvastatin treatment could prevent Aβ1-42 oligomer (AβO)-induced synaptotoxicity and memory dysfunction in rats, and to elucidate the mechanisms involved in the neuroprotective actions of atorvastatin.
Methods: SD rats were injected with AβOs (5 nmol, icv).  The rats were administrated with atorvastatin (10 mg·kg-1·d-1, po) for 2 consecutive weeks (the first dose was given 5 d before AβOs injection).  The memory impairments were evaluated with Morris water maze task.  The expression of inflammatory cytokines in the hippocampus was determined using ELISA assays.  The levels of PSD-95 and p38MAPK proteins in rat hippocampus were evaluated using Western blot analysis.  For in vitro experiments, cultured rat hippocampal neurons were treated with AβOs (50 nmol/L) for 48 h.  The expression of MAP-2 and synaptophysin in the neurons was detected with immunofluorescence. 

Results: The AβO-treated rats displayed severe memory impairments in Morris water maze tests, and markedly reduced levels of synaptic proteins synaptophysin and PSD-95, increased levels of inflammatory cytokines (IL-1β, IL-6 and TNF-α) and p38MAPK activation in the hippocampus.  All these effects were prevented or substantially attenuated by atorvastatin administration.  Pretreatment of cultured hippocampal neurons with atorvastatin (1 and 5 µmol/L) concentration-dependently attenuated the AβO-induced synaptotoxicity, including the loss of  dendritic marker MAP-2, and synaptic proteins synaptophysin and PSD-95.  Pretreatment of the cultured hippocampal neurons with the p38MAPK inhibitor SB203580 (5 µmol/L) blocked the AβO-induced loss of synaptophysin and PSD-95.

Conclusion: Atorvastatin prevents AβO-induced synaptotoxicity and memory dysfunction through a p38MAPK-dependent pathway.

 
Keywords: Alzheimer’s disease; atorvastatin; hippocampus; learning and memory; synapse; amyloid-β peptide; synaptophysin; PSD-95; cytokine; p38 MAPK
 
This work was supported by grants from the Education Commission of Liaoning Province (LT2010064) and Liaoning Medical University (2012005).
* To whom correspondence should be addressed. 
E-mail jyjinying1130@163.com 
Received 2013-10-14     Accepted 2013-12-27},
	issn = {1745-7254},	url = {http://www.chinaphar.com/article/view/5941}
}