title: [Research on EGCG improving the degenerative changes of the brain in AD model mice induced with chemical drugs].
abstract: OBJECTIVE
  To study the effect and mechanism of (-)-Epigallocatechin-3-gallate (EGCG) on the degeneretive changes of the brain in Alzheimer's disease (AD) model mice induced with chemical drugs.
  
  
  METHODS
  AD model mice were established by subcutaneously injecting with 3% D-gal at the dose of 150 mg/kg body weight once daily for 6 weeks. From the third week, the mice of D-gal + V(E) 280 U/kg group, D-gal + EGCG 2 mg/(kg x d) group and D-gal + EGCG 6 mg/(kg x d) group were intragastricly given with 5.6% V(E) at the dose of 280 IU/kg and EGCG at the dose of 2 mg/kg x d or 6 mg/kg x d respectively after injection of D-gal. The mice of control group, D-gal + dd H2O group and D-gal + oil group were administered with same volume vehicle distilled water and soybean oil respectively. The pathological changes of the brain in AD model mice were observed by HE staining analysis, the immunohistochemical analysis of beta-amyloid (Abeta) and evaluating the expression of amyloid precursor protein (APP) in the hippocampus of mice by Western blot analysis.
  
  
  RESULTS
  EGCG 2 mg/(kg x d) or 6 mg/(kg x d) 4 weeks, ig evidently released neuronal injury in the hippocampus of the AD mice induced by D-gal, and significantly reduced the express of Abeta and APP in the hippocampus of AD model mice induced by D-gal (P < 0.01).
  
  
  CONCLUSIONS
  EGCG has a protective effect on AD model mice induced by D-gal by decreasing the expression of APP and beta-Amyloid in the hippocampus of mice.
authors.affiliation: Department of Pharmacology, China Medical University, Shenyang 110001, China. hemiao_cmu@126.com
authors.forename: Miao
authors.initials: M
authors.lastname: He
authors.forename: Ming-Yan
authors.initials: MY
authors.lastname: Liu
authors.forename: Shuang
authors.initials: S
authors.lastname: Wang
authors.forename: Qiu-Shi
authors.initials: QS
authors.lastname: Tang
authors.forename: Wei-Fan
authors.initials: WF
authors.lastname: Yao
authors.forename: Hai-Shan
authors.initials: HS
authors.lastname: Zhao
authors.forename: Min-Jie
authors.initials: MJ
authors.lastname: Wei
mesh_terms: D000544:Alzheimer Disease / Q000188:drug therapy* / Q000378:metabolism / Q000473:pathology; D016229:Amyloid beta-Peptides / Q000378:metabolism*; D016564:Amyloid beta-Protein Precursor / Q000378:metabolism*; D000818:Animals; D001921:Brain / Q000187:drug effects* / Q000378:metabolism / Q000473:pathology; D002392:Catechin / Q000008:administration & dosage / Q000031:analogs & derivatives* / Q000494:pharmacology; D004195:Disease Models, Animal; D005260:Female; D005690:Galactose / Q000008:administration & dosage / Q000009:adverse effects; D005786:Gene Expression Regulation / Q000187:drug effects; D006624:Hippocampus / Q000187:drug effects / Q000378:metabolism / Q000473:pathology; D051379:Mice; D009474:Neurons / Q000378:metabolism / Q000473:pathology; D018696:Neuroprotective Agents / Q000008:administration & dosage / Q000494:pharmacology; D008517:Phytotherapy; D013662:Tea / Q000737:chemistry
chemical_list: D016229:Amyloid beta-Peptides; D016564:Amyloid beta-Protein Precursor; D018696:Neuroprotective Agents; D013662:Tea; D002392:Catechin; C045651:epigallocatechin gallate; D005690:Galactose