PMID- 25563203
OWN - NLM
STAT- MEDLINE
DCOM- 20151215
LR  - 20231213
IS  - 1573-6830 (Electronic)
IS  - 0272-4340 (Linking)
VI  - 35
IP  - 4
DP  - 2015 May
TI  - The effect of soybean isoflavone on the dysregulation of NMDA receptor signaling 
      pathway induced by beta-amyloid peptides 1-42 in rats.
PG  - 555-62
LID - 10.1007/s10571-014-0151-9 [doi]
AB  - Synaptic damage is the key factor of cognitive impairment. The purpose of this 
      study was to understand the effect of soybean isoflavone (SIF) on synaptic damage 
      induced by beta-amyloid peptide 1-42 (Abeta1-42) in rats. Adult male Wistar rats were 
      randomly divided into control, Abeta1-42, SIF, and SIF + Abeta1-42 (SIF pretreatment) 
      groups according to body weight. SIF was treated orally by gavage in SIF and SIF 
      + Abeta1-42 groups. After 14 days pretreatment with SIF or vehicle, Abeta1-42 was 
      injected into the lateral cerebral ventricle of rats in Abeta1-42 and SIF + Abeta1-42 
      groups using miniosmotic pump. The level of Abeta1-42 and the expression of 
      N-methyl-D-aspartic-acid receptor (NMDAR) were observed by immunohistochemistry. 
      Reverse transcriptase polymerase chain reaction was used to detect the mRNA 
      levels of NMDAR, calmodulin (CaM), calcium/CaM-dependent protein kinase II 
      (CaMKII), cAMP-response element binding protein (CREB), and brain-derived 
      neurotrophic factor (BDNF). The results showed that Abeta1-42 down-regulated mRNA 
      and protein expression of the NR1 and NR2B subunits of NMDAR, SIF pretreatment 
      could reverse these changes. The mRNA expression of CaM, CaMKII, CREB, and BDNF 
      were down-regulated by Abeta1-42, but they were all regulated by SIF pretreatment. 
      These results suggest that SIF pretreatment could antagonize the neuron damage in 
      rats induced by Abeta1-42, and its mechanism might be associated with the NMDA 
      receptor and CaM/CaMKII/CREB/BDNF signaling pathway, which are the synaptic 
      plasticity-related molecules.
FAU - Xi, Yuan-Di
AU  - Xi YD
AD  - School of Public Health, Capital Medical University, No. 10 Xitoutiao, You An Men 
      Wai, Beijing, 100069, China.
FAU - Ding, Juan
AU  - Ding J
FAU - Han, Jing
AU  - Han J
FAU - Zhang, Dan-Di
AU  - Zhang DD
FAU - Liu, Jin-Meng
AU  - Liu JM
FAU - Feng, Ling-Li
AU  - Feng LL
FAU - Xiao, Rong
AU  - Xiao R
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20150107
PL  - United States
TA  - Cell Mol Neurobiol
JT  - Cellular and molecular neurobiology
JID - 8200709
RN  - 0 (Amyloid beta-Peptides)
RN  - 0 (Brain-Derived Neurotrophic Factor)
RN  - 0 (Calmodulin)
RN  - 0 (Cyclic AMP Response Element-Binding Protein)
RN  - 0 (Isoflavones)
RN  - 0 (Peptide Fragments)
RN  - 0 (RNA, Messenger)
RN  - 0 (Receptors, N-Methyl-D-Aspartate)
RN  - 0 (amyloid beta-protein (1-42))
RN  - EC 2.7.11.17 (Calcium-Calmodulin-Dependent Protein Kinase Type 2)
SB  - IM
MH  - Amyloid beta-Peptides/*pharmacology/toxicity
MH  - Animals
MH  - Brain/drug effects/metabolism
MH  - Brain-Derived Neurotrophic Factor/genetics/metabolism
MH  - Calcium-Calmodulin-Dependent Protein Kinase Type 2/genetics/metabolism
MH  - Calmodulin/genetics/metabolism
MH  - Cyclic AMP Response Element-Binding Protein/genetics/metabolism
MH  - Isoflavones/*pharmacology
MH  - Male
MH  - Peptide Fragments/*toxicity
MH  - RNA, Messenger/genetics/metabolism
MH  - Rats, Wistar
MH  - Receptors, N-Methyl-D-Aspartate/genetics/*metabolism
MH  - Signal Transduction/*drug effects
MH  - Glycine max/*chemistry
EDAT- 2015/01/08 06:00
MHDA- 2015/12/17 06:00
CRDT- 2015/01/08 06:00
PHST- 2014/08/24 00:00 [received]
PHST- 2014/12/18 00:00 [accepted]
PHST- 2015/01/08 06:00 [entrez]
PHST- 2015/01/08 06:00 [pubmed]
PHST- 2015/12/17 06:00 [medline]
AID - 10.1007/s10571-014-0151-9 [doi]
PST - ppublish
SO  - Cell Mol Neurobiol. 2015 May;35(4):555-62. doi: 10.1007/s10571-014-0151-9. Epub 
      2015 Jan 7.