Anthocyanins control neuroinflammation and consequent memory dysfunction in mice exposed to lipopolysaccharide

被引:57
作者
Carvalho, Fabiano B. [1 ]
Gutierres, Jessie M. [1 ]
Bueno, Andressa [2 ]
Agostinho, Paula [3 ]
Zago, Adriana M. [1 ]
Vieira, Juliano [1 ]
Fruhauf, Pamela [4 ]
Cechella, Jose L. [1 ]
Nogueira, Cristina Wayne [1 ]
Oliveira, Sara M. [1 ]
Rizzi, Caroline [5 ]
Spanevello, Roselia M. [1 ,6 ]
Duarte, Marta M. F. [7 ]
Duarte, Thiago [4 ]
Dellagostin, Odir A. [5 ]
Andrade, Cinthia M. [1 ,2 ]
机构
[1] Univ Fed Santa Maria, Dept Bioquim & Biol Mol, Ctr Ciencias Nat & Exatas, Programa Posgrad Ciencias Biol Bioquim Toxicol, BR-97105900 Santa Maria, RS, Brazil
[2] Univ Fed Santa Maria, Dept Pequenos Animais, Ctr Ciencias Rurais, Programa Posgrad Med Vet, BR-97105900 Santa Maria, RS, Brazil
[3] Univ Coimbra, CNC Ctr Neurosci & Cell Biol, Portugal FMUC Fac Med, P-3004517 Coimbra, Portugal
[4] Univ Fed Santa Maria, Ctr Ciencias Saude, Programa Posgrad Farmacol, BR-97105900 Santa Maria, RS, Brazil
[5] Univ Fed Pelotas, Programa Posgrad Biotecnol, Ctr Desenvolvimento Tecnol, Unidade Biotecnologia, Campus Univ, BR-96010900 Pelotas, RS, Brazil
[6] Univ Fed Pelotas, Programa Posgrad Bioquim & Bioprospeccao, Ctr Ciencias Quim Farmaceut & Alimentos, Campus Univ, BR-96010900 Pelotas, RS, Brazil
[7] Univ Luterana Brasil, Dept Ciencias Saude, BR-97020001 Santa Maria, RS, Brazil
关键词
Neuroinflammation; Anthocyanins; Memory; Oxidative stress; Microglia; Interleukins; ADENOSINE A(2A) RECEPTORS; TERM COGNITIVE IMPAIRMENT; CENTRAL-NERVOUS-SYSTEM; NF-KAPPA-B; OXIDATIVE STRESS; NA+; K+-ATPASE ACTIVITY; ALZHEIMERS-DISEASE; SICKNESS BEHAVIOR; RAT HIPPOCAMPUS; PROINFLAMMATORY MEDIATORS;
D O I
10.1007/s12035-016-9900-8
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
Peripheral inflammatory stimuli may activate a brain neuroinflammatory processes with consequences in brain function. The present study investigated if anthocyanins (ANT) consumption was able to prevent the memory loss, the neuronal damage, and the neuroinflammatory processes triggered by the intraperitoneal lipopolysaccharide (LPS) administration. C57BL6 male mice were treated with ANT (30-100 mg/kg by gavage). With a single dose or during 10 days, before be challenged with LPS (250 mu g/kg intraperitoneally single administration), a classical inductor of inflammation. The data obtained showed that ANT was able to confer protection against the memory impairment after 10 days of ANT treatment (100 mg/kg). This phytonutrient also prevented the hypothermia episode induced by LPS. Moreover, ANT prevented the increase in protein carbonyl, NOx, and MDA levels in the hippocampus and cerebral cortex (4 and 24 h) in animal challenged with LPS. ANT showed a protective effect on the increase in the pro-inflammatory cytokines content, especially Interleukin (IL)-1 beta, tumoral necrosis factor-alpha and on the reduction of IL-10 induced by LPS. ANT 100 mg/kg prevented the infiltration of peripheral immune cells in the hippocampus at 24 h post-LPS administration. In parallel, LPS increased the activity of myeloperoxidase in cortex and hippocampus, and ANT prevented this effect, also reducing microglia (Iba-1) and astrocyte (GFAP) immunoreactivity. Thus, our data support that ANT are a promising therapeutic component against brain disorders associated with process of neuroinflammation.
引用
收藏
页码:3350 / 3367
页数:18
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