PMID- 24488601
OWN - NLM
STAT- MEDLINE
DCOM- 20150406
LR  - 20211021
IS  - 1559-1166 (Electronic)
IS  - 0895-8696 (Linking)
VI  - 53
IP  - 4
DP  - 2014 Aug
TI  - Neuroprotective effects of 3,6'-disinapoyl sucrose through increased BDNF levels 
      and CREB phosphorylation via the CaMKII and ERK1/2 pathway.
PG  - 600-7
LID - 10.1007/s12031-013-0226-y [doi]
AB  - 3,6'-Disinapoyl sucrose (DISS) is an oligosaccharide ester natural product 
      originating from the root of wild Polygala tenuifolia. Our previous reports 
      suggested that DISS can have neuroprotective effects and antidepressive activity 
      in rats, at least in part, by increased expression of cyclic AMP response element 
      (CRE)-binding protein (CREB) and its downstream target protein, brain-derived 
      neurotrophic factor (BDNF). The aim of the present study was to explore the 
      mechanism of DISS-modulated BDNF and CREB expression. In this study, we confirmed 
      its neuroprotective effect by showing that DISS, at concentrations above 30 muM, 
      could promote the neuron cell viability and protected the glutamate and 
      H2O2-induced toxicity in the human neuroblastoma (SH-SY5Y) cell line. DISS 
      treatment also increased acute (from 15 to 30 min) BDNF expression and CREB 
      phosphorylation in a dose-dependent manner. Pharmacological inhibition of 
      mitogen-activated protein kinase 1 (ERK1/2), CaMKII, and Trk (with U0126, KN93, 
      or K252a, respectively) partially attenuated the stimulatory effect of DISS on 
      phospho-CREB and BDNF expression; however, it was not inhibited by 
      pharmacological inhibition of PKA or PI3K (with H89 and LY294002, respectively). 
      The results are consistent with the effects of DISS on CRE-directed gene 
      transcription, as U0126 and KN-93 treatment also blocked the DISS-induced 
      expression of the CRE-luciferase reporter gene. The results from the present 
      study suggest that DISS-mediated regulation of BDNF gene expression is associated 
      with CREB-mediated transcription of BDNF and upstream activation of ERK1/2 and 
      CaMKII. Finally, DISS may exert neuroprotective and antidepressant effects 
      through these signaling pathways in neuronal cells.
FAU - Hu, Yuan
AU  - Hu Y
AD  - Department of Clinical Pharmacology, Pharmacy Care Center, Chinese PLA General 
      Hospital, No. 28 FuXing Road, Beijing, 100853, People's Republic of China.
FAU - Liu, Ming-Yue
AU  - Liu MY
FAU - Liu, Ping
AU  - Liu P
FAU - Dong, XianZhe
AU  - Dong X
FAU - Boran, Aislyn D W
AU  - Boran AD
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20140204
PL  - United States
TA  - J Mol Neurosci
JT  - Journal of molecular neuroscience : MN
JID - 9002991
RN  - 0 (3,6'-disinapoylsucrose)
RN  - 0 (Brain-Derived Neurotrophic Factor)
RN  - 0 (Coumaric Acids)
RN  - 0 (Cyclic AMP Response Element-Binding Protein)
RN  - 0 (Neuroprotective Agents)
RN  - 0 (Phosphoinositide-3 Kinase Inhibitors)
RN  - 0 (Protein Kinase Inhibitors)
RN  - 57-50-1 (Sucrose)
RN  - EC 2.7.11.11 (Cyclic AMP-Dependent Protein Kinases)
RN  - EC 2.7.11.17 (Calcium-Calmodulin-Dependent Protein Kinase Type 2)
SB  - IM
MH  - Brain-Derived Neurotrophic Factor/genetics/*metabolism
MH  - Calcium-Calmodulin-Dependent Protein Kinase Type 2/antagonists & 
      inhibitors/*metabolism
MH  - Cell Line, Tumor
MH  - Coumaric Acids/*pharmacology
MH  - Cyclic AMP Response Element-Binding Protein/genetics/*metabolism
MH  - Cyclic AMP-Dependent Protein Kinases/antagonists & inhibitors/metabolism
MH  - Humans
MH  - *MAP Kinase Signaling System
MH  - Neurons/drug effects/metabolism
MH  - Neuroprotective Agents/*pharmacology
MH  - Phosphatidylinositol 3-Kinases/metabolism
MH  - Phosphoinositide-3 Kinase Inhibitors
MH  - Phosphorylation
MH  - Protein Kinase Inhibitors/pharmacology
MH  - Sucrose/*analogs & derivatives/pharmacology
EDAT- 2014/02/04 06:00
MHDA- 2015/04/07 06:00
CRDT- 2014/02/04 06:00
PHST- 2013/11/11 00:00 [received]
PHST- 2013/12/29 00:00 [accepted]
PHST- 2014/02/04 06:00 [entrez]
PHST- 2014/02/04 06:00 [pubmed]
PHST- 2015/04/07 06:00 [medline]
AID - 10.1007/s12031-013-0226-y [doi]
PST - ppublish
SO  - J Mol Neurosci. 2014 Aug;53(4):600-7. doi: 10.1007/s12031-013-0226-y. Epub 2014 
      Feb 4.