PMID- 23454192
OWN - NLM
STAT- MEDLINE
DCOM- 20131022
LR  - 20161125
IS  - 1872-9754 (Electronic)
IS  - 0197-0186 (Linking)
VI  - 62
IP  - 6
DP  - 2013 May
TI  - Lectin from Canavalia brasiliensis (ConBr) protects hippocampal slices against 
      glutamate neurotoxicity in a manner dependent of PI3K/Akt pathway.
PG  - 836-42
LID - S0197-0186(13)00065-X [pii]
LID - 10.1016/j.neuint.2013.02.020 [doi]
AB  - The excitotoxicity induced by excessive activation of the glutamatergic 
      neurotransmission pathway is involved in several neuropathologies. In this sense, 
      molecules that prevent the release of glutamate or the excessive activation of 
      its receptors can be useful in preventing the neuronal cell death observed in 
      these diseases. Lectins are proteins capable of reversible binding to the 
      carbohydrates in glycoconjugates, and some have been used in the study and 
      purification of glutamate receptors. ConBr is a mannose/glucose-binding lectin 
      purified from Canavalia brasiliensis seeds. In the present study, we aimed to 
      evaluate the neuroprotective activity of ConBr against glutamate-induced 
      excitotoxicity. Hippocampal slices were isolated from adult male mice and 
      incubated for 6h in Krebs saline/DMEM buffer alone (control), in the presence of 
      glutamate or glutamate plus ConBr. The phosphorylation of Akt and mitogen 
      activated protein kinases (MAPKs) such as ERK1/2, p38(MAPK) and JNK1/2/3 was 
      evaluated with western blotting. The results indicate that glutamate provoked a 
      reduction in the hippocampal slice viability (-25%), diminished the 
      phosphorylation of Akt and augmented p38(MAPK) and ERK1 phosphorylation. No 
      changes were observed in the phosphorylation of JNK1/2/3 or ERK2. Notably, ConBr, 
      through a mechanism dependent on carbohydrate interaction, prevented the 
      reduction of cell viability and Akt phosphorylation induced by glutamate. 
      Furthermore, in the presence of the PI3K inhibitor LY294002, ConBr was unable to 
      reverse glutamate neurotoxicity. Taken together, our data suggest that the 
      neuroprotective effect of ConBr against glutamate neurotoxicity requires 
      oligosaccharide interaction and is dependent on the PI3K/Akt pathway.
CI  - Copyright (c) 2013 Elsevier Ltd. All rights reserved.
FAU - Jacques, Amanda V
AU  - Jacques AV
AD  - Departamento de Bioquimica, Centro de Ciencias Biologicas, Universidade Federal 
      de Santa Catarina, SC, Brazil.
FAU - Rieger, Debora K
AU  - Rieger DK
FAU - Maestri, Mariana
AU  - Maestri M
FAU - Lopes, Mark W
AU  - Lopes MW
FAU - Peres, Tanara V
AU  - Peres TV
FAU - Goncalves, Filipe M
AU  - Goncalves FM
FAU - Pedro, Daniela Z
AU  - Pedro DZ
FAU - Tasca, Carla I
AU  - Tasca CI
FAU - Lopez, Manuela G
AU  - Lopez MG
FAU - Egea, Javier
AU  - Egea J
FAU - Nascimento, Kyria S
AU  - Nascimento KS
FAU - Cavada, Benildo S
AU  - Cavada BS
FAU - Leal, Rodrigo B
AU  - Leal RB
LA  - eng
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, Non-U.S. Gov't
DEP - 20130226
PL  - England
TA  - Neurochem Int
JT  - Neurochemistry international
JID - 8006959
RN  - 0 (Chromones)
RN  - 0 (Enzyme Inhibitors)
RN  - 0 (Excitatory Amino Acid Antagonists)
RN  - 0 (Morpholines)
RN  - 0 (Neuroprotective Agents)
RN  - 0 (Plant Lectins)
RN  - 0 (Tetrazolium Salts)
RN  - 0 (Thiazoles)
RN  - 0 (lectin, Canavalia)
RN  - 31M2U1DVID (2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one)
RN  - 3KX376GY7L (Glutamic Acid)
RN  - EC 2.7.1.- (Phosphatidylinositol 3-Kinases)
RN  - EC 2.7.11.1 (Oncogene Protein v-akt)
RN  - EC 2.7.11.24 (Mitogen-Activated Protein Kinases)
RN  - EUY85H477I (thiazolyl blue)
SB  - IM
MH  - Animals
MH  - Blotting, Western
MH  - Canavalia/*chemistry
MH  - Carbohydrate Metabolism/drug effects
MH  - Cell Survival/drug effects
MH  - Chromones/pharmacology
MH  - Enzyme Inhibitors/pharmacology
MH  - *Excitatory Amino Acid Antagonists
MH  - Glutamic Acid/*toxicity
MH  - Hippocampus/*drug effects/pathology
MH  - In Vitro Techniques
MH  - Male
MH  - Mice
MH  - Mitogen-Activated Protein Kinases/physiology
MH  - Morpholines/pharmacology
MH  - *Neuroprotective Agents
MH  - Oncogene Protein v-akt/*physiology
MH  - Phosphatidylinositol 3-Kinases/*physiology
MH  - Phosphorylation
MH  - Plant Lectins/chemistry/isolation & purification/*pharmacology
MH  - Signal Transduction/*drug effects
MH  - Tetrazolium Salts
MH  - Thiazoles
EDAT- 2013/03/05 06:00
MHDA- 2013/10/23 06:00
CRDT- 2013/03/05 06:00
PHST- 2012/07/31 00:00 [received]
PHST- 2013/02/05 00:00 [revised]
PHST- 2013/02/08 00:00 [accepted]
PHST- 2013/03/05 06:00 [entrez]
PHST- 2013/03/05 06:00 [pubmed]
PHST- 2013/10/23 06:00 [medline]
AID - S0197-0186(13)00065-X [pii]
AID - 10.1016/j.neuint.2013.02.020 [doi]
PST - ppublish
SO  - Neurochem Int. 2013 May;62(6):836-42. doi: 10.1016/j.neuint.2013.02.020. Epub 
      2013 Feb 26.