Long-term but Not Short-term Aspirin Treatment Attenuates Diabetes-associated Learning and Memory Decline in Mice

被引:12
作者
Wang, T. [1 ,2 ]
Fu, F. H. [2 ]
Han, B. [2 ]
Zhang, L. M. [2 ]
Zhang, X. M. [1 ]
机构
[1] Shandong Univ, Sch Med, Dept Pharmacol, Jinan 250012, Shandong, Peoples R China
[2] Yantai Univ, Sch Pharm, Dept Pharmacol, Yantai 264005, Peoples R China
关键词
aspirin; diabetes; learning; memory; ALZHEIMERS-DISEASE; ANTIINFLAMMATORY DRUGS; ACETYLCHOLINESTERASE ACTIVITY; INFLAMMATORY PROCESSES; TRANSGENIC MICE; EXPRESSION; MELLITUS; RISK; DEMENTIA;
D O I
10.1055/s-0030-1261933
中图分类号
R5 [内科学];
学科分类号
100201 [内科学];
摘要
Increasing studies have shown that the patients with diabetes mellitus have an increased risk of cognitive impairment, dementia, and neurodegeneration. The present study was designed to evaluate the effect of aspirin on diabetes-associated learning and memory decline in mice. Diabetes was induced by a single intraperitoneal injection of streptozocin (150 mg/kg body weight) in C57BL/6 mice. The mice were administered with aspirin at a dose of 30 mg/kg by intragastric administration once a day for 1, 4 or 8 weeks respectively. 8 weeks after aspirin or vehicle treatment, the effect of aspirin on diabetes-associated learning and memory decline in mice was investigated by evaluating the mean escape latency and the percentage of time spent in target quadrant. The TNF-alpha, IL-1 beta contents, and acetylcholinesterase activity in hippocampus were assayed as well. The results showed that administration with aspirin for 4 weeks or 8 weeks significantly reduced the mean escape latency, the acetylcholinesterase activity, the TNF-alpha, IL-1 beta levels and increased the percentage of time spent in target quadrant. However, treatment with aspirin for 1 week did not ameliorate diabetes-associated learning and memory decline. The present study demonstrated that long-term aspirin treatment attenuates diabetes-associated learning and memory decline in mice, and that the effect of aspirin was related to its anti-inflammatory potency.
引用
收藏
页码:36 / 40
页数:5
相关论文
共 26 条
[1]
Akassoglou K, 1997, J IMMUNOL, V158, P438
[2]
Cell mediators of inflammation in the Alzheimer disease brain [J].
Akiyama, H ;
Arai, T ;
Kondo, H ;
Tanno, E ;
Haga, C ;
Ikeda, K .
ALZHEIMER DISEASE & ASSOCIATED DISORDERS, 2000, 14 :S47-S53
[3]
Diabetes mellitus and risk of developing Alzheimer disease - Results from the Framingham study [J].
Akomolafe, Abimbola ;
Beiser, Alexa ;
Meigs, Phdjames B. ;
Au, Rhoda ;
Green, Robert C. ;
Farrer, Lindsay A. ;
Wolf, Philip A. ;
Seshadri, Sudha .
ARCHIVES OF NEUROLOGY, 2006, 63 (11) :1551-1555
[4]
Barnum SR, 1996, GLIA, V18, P107, DOI 10.1002/(SICI)1098-1136(199610)18:2<107::AID-GLIA3>3.0.CO
[5]
2-Y
[6]
Linking stress to inflammation [J].
Bierhaus, Angelika ;
Humpert, Per M. ;
Nawroth, Peter P. .
ANESTHESIOLOGY CLINICS OF NORTH AMERICA, 2006, 24 (02) :325-+
[7]
Breitner JCS, 1996, NEUROBIOL AGING, V17, P789
[8]
Inflammation: the link between insulin resistance, obesity and diabetes [J].
Dandona, P ;
Aljada, A ;
Bandyopadhyay, A .
TRENDS IN IMMUNOLOGY, 2004, 25 (01) :4-7
[9]
EXPRESSION OF THE ALZHEIMER AMYLOID-PROMOTING FACTOR ANTICHYMOTRYPSIN IS INDUCED IN HUMAN ASTROCYTES BY IL-1 [J].
DAS, S ;
POTTER, H .
NEURON, 1995, 14 (02) :447-456
[10]
A NEW AND RAPID COLORIMETRIC DETERMINATION OF ACETYLCHOLINESTERASE ACTIVITY [J].
ELLMAN, GL ;
COURTNEY, KD ;
ANDRES, V ;
FEATHERSTONE, RM .
BIOCHEMICAL PHARMACOLOGY, 1961, 7 (02) :88-&