PMID- 23944053
OWN - NLM
STAT- MEDLINE
DCOM- 20130917
LR  - 20161125
IS  - 1001-5302 (Print)
IS  - 1001-5302 (Linking)
VI  - 38
IP  - 9
DP  - 2013 May
TI  - [Effects of icariin on beta-amyloid and neurotrophic factors in brain of 
      mitochondrial deficiency model rats].
PG  - 1285-9
AB  - The purpose of the present study was to investigate the effects of icariin (ICA) 
      on the content of beta-amyloid (Abeta) and the expression of neurotrophic factors 
      in the brain of mitochondrial deficiency model rats. SD rats were infused 
      subcutaneously with sodium azide, which is an inhibitor of mitochondrial 
      respiratory chain complex IV, via a minipump (0. 5 mg . kg-1 h-1) for 28 days to 
      establish the mitochondrial deficiency animal model. The activity of 
      mitochondrial respiratory chain complex IV (i. e. cytochrome C oxidase, COX) in 
      hippocampus was measured by biochemical methods. ELISA method was used to detect 
      the content of Abeta in the brain. The expression of neurotrophic factors was 
      detected by Western blot and immunohistochemistry methods. Image analysis was 
      performed by Image-pro software. The results showed that chronic infusion of 
      sodium azide by minipump induced a significant decrease in the activity of 
      mitochondrial cytochrome C oxidase, an obvious increase in the content of Abeta, 
      and a marked decline in the expression of nerve growth factor (NGF), 
      brain-derived neurotrophic factor (BDNF) and its receptor TrkB in the brain of 
      rats. Intragastrical administration of ICA (12 or 36 mg . kg-l) significantly 
      ameliorated all these abnormalities in the model rats. In conclusion, ICA can 
      increase mitochondrial activity, inhibit Abeta production, and enhance the 
      expression of neurotrophic factors in the brain of model rats induced by sodium 
      azide. The results suggested that ICA may have beneficial prospect for the 
      treatment of Alzheimer's disease.
FAU - Zhang, Ru-Yi
AU  - Zhang RY
AD  - Department of Pharmacology, Xuanwu Hospital of Capital Medical University, Key 
      Laboratory for Neurodegenerative Diseases of Ministry of Education, Beijing 
      100053, China. ruyiz2@sina.com
FAU - Zhang, Li
AU  - Zhang L
FAU - Ai, Hou-Xi
AU  - Ai HX
FAU - Zhang, Lan
AU  - Zhang L
FAU - Li, Lin
AU  - Li L
LA  - chi
PT  - Journal Article
PL  - China
TA  - Zhongguo Zhong Yao Za Zhi
JT  - Zhongguo Zhong yao za zhi = Zhongguo zhongyao zazhi = China journal of Chinese 
      materia medica
JID - 8913656
RN  - 0 (Amyloid)
RN  - 0 (Brain-Derived Neurotrophic Factor)
RN  - 0 (Flavonoids)
RN  - 0 (Nerve Growth Factors)
RN  - 9061-61-4 (Nerve Growth Factor)
RN  - EC 2.7.10.1 (Receptor, trkB)
RN  - VNM47R2QSQ (icariin)
SB  - IM
MH  - Amyloid/*metabolism
MH  - Animals
MH  - Brain/*drug effects/*metabolism
MH  - Brain-Derived Neurotrophic Factor/metabolism
MH  - Disease Models, Animal
MH  - Enzyme-Linked Immunosorbent Assay
MH  - Flavonoids/*pharmacology/therapeutic use
MH  - Mitochondria/drug effects/metabolism/pathology
MH  - Mitochondrial Diseases/drug therapy/metabolism
MH  - Nerve Growth Factor/metabolism
MH  - Nerve Growth Factors/*metabolism
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - Receptor, trkB/metabolism
EDAT- 2013/08/16 06:00
MHDA- 2013/09/18 06:00
CRDT- 2013/08/16 06:00
PHST- 2013/08/16 06:00 [entrez]
PHST- 2013/08/16 06:00 [pubmed]
PHST- 2013/09/18 06:00 [medline]
PST - ppublish
SO  - Zhongguo Zhong Yao Za Zhi. 2013 May;38(9):1285-9.