title: [Influence of scutellarin on oxidative stress and neuronal apoptosis of rats with dementia].
abstract: OBJECTIVE
  To investigate the influence of Scutellarin on the oxidative stress and neuronal apoptosis in rats with dementia and to reveal therapeutic mechanism of the drug to Alzheimer's disease.
  
  
  METHODS
  Wistar rats were randomly divided into 5 groups: normal control group, sham group, model group,scutellarin group and positive control group. The animal model with dementia was by bilateral ventricle injection with beta-amyloid peptide (AP) 25-35 and intraperitoneal injection with D-galactose. Learning and memory ability of rats were detected by Morris Water Maze test; Histopathology of the cerebral cortex and hippocampus were observed under light microscope; Changes of Nissl's body in the hippocampus were survey by Nissl staining; The activities of SOD and MAO were detected by xanthinoxidase method and chemical method, respectively, and neuronal apoptosis was measured using flow cytometry.
  
  
  RESULTS
  Compared with control group and sham group, the ability of learning and memory of the rats in model group was decreased; Neuropathological changes were observed in the hippocampus; The activity of SOD was decreased while the activity of MAO increased in brain tissues; Neuronal apoptosis percentage was increased. After treated with Scutellarin, learning and memory ability of rats with dementia was improved; The pathologic changes were alleviated; The activity of SOD was up-regulation and the activity of MAO was decreased; Neuronal apoptosis percentage was declined. No significant difference between the scutellarin group and positive drug control group was found.
  
  
  CONCLUSIONS
  Scutellarin might play an therapeutic role by inhibiting oxidative stress and apoptosis in AD treatment.
authors.affiliation: The Dept. of Pathology and Molecular Biology, Guiyang Medical College, Guiyang 550004, China. lilly_g@yahoo.cn
authors.forename: Li-li
authors.initials: LL
authors.lastname: Guo
authors.forename: Jie
authors.initials: J
authors.lastname: Deng
authors.forename: Yong-lin
authors.initials: YL
authors.lastname: Wang
authors.forename: Yong
authors.initials: Y
authors.lastname: Huang
authors.forename: Zhi-zhong
authors.initials: ZZ
authors.lastname: Guan
mesh_terms: D000544:Alzheimer Disease / Q000188:drug therapy / Q000473:pathology; D016229:Amyloid beta-Peptides; D000818:Animals; D047310:Apigenin / Q000494:pharmacology* / Q000627:therapeutic use; D017209:Apoptosis / Q000187:drug effects*; D030023:Asarum / Q000737:chemistry; D002540:Cerebral Cortex / Q000378:metabolism* / Q000473:pathology; D003704:Dementia / Q000188:drug therapy / Q000378:metabolism / Q000473:pathology*; D004195:Disease Models, Animal; D005260:Female; D005965:Glucuronates / Q000494:pharmacology* / Q000627:therapeutic use; D006624:Hippocampus / Q000378:metabolism / Q000473:pathology; D008297:Male; D018782:Maze Learning / Q000187:drug effects; D008568:Memory / Q000187:drug effects; D009474:Neurons / Q000378:metabolism / Q000473:pathology; D018696:Neuroprotective Agents / Q000494:pharmacology* / Q000627:therapeutic use; D018384:Oxidative Stress / Q000187:drug effects*; D010446:Peptide Fragments; D011897:Random Allocation; D051381:Rats; D017208:Rats, Wistar; D013482:Superoxide Dismutase / Q000378:metabolism
chemical_list: D016229:Amyloid beta-Peptides; D005965:Glucuronates; D018696:Neuroprotective Agents; D010446:Peptide Fragments; C074636:amyloid beta-protein (25-35); C484876:scutellarin; D047310:Apigenin; D013482:Superoxide Dismutase