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10.1074/jbc.M116.763813

http://scihub22266oqcxt.onion/10.1074/jbc.M116.763813
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suck abstract from ncbi


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pmid28087694
      J+Biol+Chem 2017 ; 292 (9 ): 3720-3728
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  • Iso-?-acids, Bitter Components of Beer, Prevent Inflammation and Cognitive Decline Induced in a Mouse Model of Alzheimer s Disease #MMPMID28087694
  • Ano Y ; Dohata A ; Taniguchi Y ; Hoshi A ; Uchida K ; Takashima A ; Nakayama H
  • J Biol Chem 2017[Mar]; 292 (9 ): 3720-3728 PMID28087694 show ga
  • Alongside the rapid growth in aging populations worldwide, prevention and therapy for age-related memory decline and dementia are in great demand to maintain a long, healthy life. Here we found that iso-?-acids, hop-derived bitter compounds in beer, enhance microglial phagocytosis and suppress inflammation via activation of the peroxisome proliferator-activated receptor ?. In normal mice, oral administration of iso-?-acids led to a significant increase both in CD11b and CD206 double-positive anti-inflammatory type microglia (p < 0.05) and in microglial phagocytosis in the brain. In Alzheimer's model 5xFAD mice, oral administration of iso-?-acids resulted in a 21% reduction in amyloid ? in the cerebral cortex as observed by immunohistochemical analysis, a significant reduction in inflammatory cytokines such as IL-1? and chemokines including macrophage inflammatory protein-1? in the cerebral cortex (p < 0.05) and a significant improvement in a novel object recognition test (p < 0.05), as compared with control-fed 5xFAD mice. The differences in iso-?-acid-fed mice were due to the induction of microglia to an anti-inflammatory phenotype. The present study is the first to report that amyloid ? deposition and inflammation are suppressed in a mouse model of Alzheimer's disease by a single component, iso-?-acids, via the regulation of microglial activation. The suppression of neuroinflammation and improvement in cognitive function suggests that iso-?-acids contained in beer may be useful for the prevention of dementia.
  • |*Beer [MESH]
  • |Acids/*chemistry [MESH]
  • |Administration, Oral [MESH]
  • |Alzheimer Disease/genetics/*metabolism [MESH]
  • |Amyloid beta-Peptides/metabolism [MESH]
  • |Animals [MESH]
  • |Anti-Inflammatory Agents/chemistry [MESH]
  • |Blood-Brain Barrier [MESH]
  • |CD11b Antigen/metabolism [MESH]
  • |Cell Separation [MESH]
  • |Cells, Cultured [MESH]
  • |Chemokine CCL3/metabolism [MESH]
  • |Chromatography, High Pressure Liquid [MESH]
  • |Chromatography, Liquid [MESH]
  • |Cognitive Dysfunction/*prevention & control [MESH]
  • |Disease Models, Animal [MESH]
  • |Humans [MESH]
  • |Immunohistochemistry [MESH]
  • |Inflammation/*prevention & control [MESH]
  • |Lectins, C-Type/metabolism [MESH]
  • |Mannose Receptor [MESH]
  • |Mannose-Binding Lectins/metabolism [MESH]
  • |Mice [MESH]
  • |Mice, Transgenic [MESH]
  • |Microglia/metabolism [MESH]
  • |Phagocytosis [MESH]
  • |Phenotype [MESH]
  • |Receptors, Cell Surface/metabolism [MESH]


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