title: Ameliorative effects of baicalein on an amyloid-β induced Alzheimer's disease rat model: a proteomics study.
abstract: BACKGROUND
  Alzheimer's disease (AD) is the most common type of age-related dementia. Effective anti-AD drugs against amyloid-β-protein-induced cognitive impairment are still lacking. Baicalein is the main component of Radix Scutellariae and has neuroprotective properties. In this study, we provide further insights into pharmacotherapy mechanisms and potential targets of baicalein in AD.
  
  
  OBJECTIVE
  To investigate the therapeutic effects and mechanism of action of baicalein in an AD rat model.
  
  
  METHODS
  Male rats were intracerebroventricularly injected with amyloid-β(Aβ) 1-40, and baicalein was orally administered. The therapeutic effect was evaluated with the Morris water maze test, and the mechanism of action was studied using a proteomics approach and western blotting.
  
  
  RESULTS
  Baicalein treatment significantly attenuated Aβ1-40-induced abnormalities in cognitive function. Additionally, the expression levels of 24 proteins in the cerebral cortex and hippocampus were significantly influenced by baicalein; approximately 50% of these proteins are related to energy metabolism and neurotransmission, whereas others are related to anti-apoptosis, anti-oxidation, the stress response, protein phosphorylation, the cytoskeleton, phospholipid metabolism and cell signaling. The expression of these proteins was increased, except for the proteins related to the cytoskeleton. The changes in the expression of 2 proteins were confirmed by western blotting.
  
  
  CONCLUSIONS
  Baicalein ameliorates the Aβ1-40-induced dementia in rats and may be a novel and promising drug for the treatment of AD. The therapeutic mechanism may be related to modulation of a number of processes, mainly through the promotion of energy metabolism and neurotransmission, with the additional promotion of anti-apoptosis, anti-oxidation, protein phosphorylation, etc.
authors.forename: Dongfeng
authors.initials: D
authors.lastname: Wei
authors.forename: Jinfu
authors.initials: J
authors.lastname: Tang
authors.forename: Weiguo
authors.initials: W
authors.lastname: Bai
authors.forename: Yongyan
authors.initials: Y
authors.lastname: Wang
authors.affiliation: State Key Laboratory of Cognitive Neuroscience and Learning & IDG/McGovern Institute for Brain Research, Beijing Normal University, Beijing 100875, China. zhang_rzs@bnu.edu.cn.
authors.forename: Zhanjun
authors.initials: Z
authors.lastname: Zhang
mesh_terms: D000544:Alzheimer Disease / Q000188:drug therapy* / Q000503:physiopathology; D016229:Amyloid beta-Peptides; D000818:Animals; D015153:Blotting, Western; D002540:Cerebral Cortex / Q000187:drug effects* / Q000503:physiopathology; D004195:Disease Models, Animal; D015180:Electrophoresis, Gel, Two-Dimensional; D044950:Flavanones / Q000737:chemistry / Q000494:pharmacology*; D006624:Hippocampus / Q000187:drug effects* / Q000503:physiopathology; D008297:Male; D018782:Maze Learning / Q000187:drug effects / Q000502:physiology; D015394:Molecular Structure; D018696:Neuroprotective Agents / Q000737:chemistry / Q000494:pharmacology*; D010446:Peptide Fragments; D040901:Proteomics / Q000379:methods; D011897:Random Allocation; D017207:Rats, Sprague-Dawley; D019032:Spectrometry, Mass, Matrix-Assisted Laser Desorption-Ionization
chemical_list: D016229:Amyloid beta-Peptides; D044950:Flavanones; D018696:Neuroprotective Agents; D010446:Peptide Fragments; C078592:amyloid beta-protein (1-40); C006680:baicalein