PMID- 21823483
OWN - NLM
STAT- MEDLINE
DCOM- 20111128
LR  - 20161125
IS  - 1001-4454 (Print)
IS  - 1001-4454 (Linking)
VI  - 34
IP  - 2
DP  - 2011 Feb
TI  - [Influence of scutellarin on oxidative stress and neuronal apoptosis of rats with 
      dementia].
PG  - 237-41
AB  - 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. CONCLUSION: Scutellarin might play an therapeutic role by 
      inhibiting oxidative stress and apoptosis in AD treatment.
FAU - Guo, Li-li
AU  - Guo LL
AD  - The Dept. of Pathology and Molecular Biology, Guiyang Medical College, Guiyang 
      550004, China. lilly_g@yahoo.cn
FAU - Deng, Jie
AU  - Deng J
FAU - Wang, Yong-lin
AU  - Wang YL
FAU - Huang, Yong
AU  - Huang Y
FAU - Guan, Zhi-zhong
AU  - Guan ZZ
LA  - chi
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - China
TA  - Zhong Yao Cai
JT  - Zhong yao cai = Zhongyaocai = Journal of Chinese medicinal materials
JID - 9426370
RN  - 0 (Amyloid beta-Peptides)
RN  - 0 (Glucuronates)
RN  - 0 (Neuroprotective Agents)
RN  - 0 (Peptide Fragments)
RN  - 0 (amyloid beta-protein (25-35))
RN  - 16IGP0ML9A (scutellarin)
RN  - 7V515PI7F6 (Apigenin)
RN  - EC 1.15.1.1 (Superoxide Dismutase)
SB  - IM
MH  - Alzheimer Disease/drug therapy/pathology
MH  - Amyloid beta-Peptides
MH  - Animals
MH  - Apigenin/*pharmacology/therapeutic use
MH  - Apoptosis/*drug effects
MH  - Asarum/chemistry
MH  - Cerebral Cortex/*metabolism/pathology
MH  - Dementia/drug therapy/metabolism/*pathology
MH  - Disease Models, Animal
MH  - Female
MH  - Glucuronates/*pharmacology/therapeutic use
MH  - Hippocampus/metabolism/pathology
MH  - Male
MH  - Maze Learning/drug effects
MH  - Memory/drug effects
MH  - Neurons/metabolism/pathology
MH  - Neuroprotective Agents/*pharmacology/therapeutic use
MH  - Oxidative Stress/*drug effects
MH  - Peptide Fragments
MH  - Random Allocation
MH  - Rats
MH  - Rats, Wistar
MH  - Superoxide Dismutase/metabolism
EDAT- 2011/08/10 06:00
MHDA- 2011/12/13 00:00
CRDT- 2011/08/10 06:00
PHST- 2011/08/10 06:00 [entrez]
PHST- 2011/08/10 06:00 [pubmed]
PHST- 2011/12/13 00:00 [medline]
PST - ppublish
SO  - Zhong Yao Cai. 2011 Feb;34(2):237-41.