PMID- 28679060
OWN - NLM
STAT- MEDLINE
DCOM- 20180614
LR  - 20211204
IS  - 1205-7541 (Electronic)
IS  - 0008-4212 (Linking)
VI  - 95
IP  - 12
DP  - 2017 Dec
TI  - Protective effects of a green tea polyphenol, epigallocatechin-3-gallate, against 
      sevoflurane-induced neuronal apoptosis involve regulation of CREB/BDNF/TrkB and 
      PI3K/Akt/mTOR signalling pathways in neonatal mice.
PG  - 1396-1405
LID - 10.1139/cjpp-2016-0333 [doi]
AB  - Epigallocatechin-3-gallate (EGCG), a polyphenol in green tea, is an effective 
      antioxidant and possesses neuroprotective effects. Brain-derived neurotrophic 
      factor (BDNF) and cyclic AMP response element-binding protein (CREB) are crucial 
      for neurogenesis and synaptic plasticity. In this study, we aimed to assess the 
      protective effects of EGCG against sevoflurane-induced neurotoxicity in neonatal 
      mice. Distinct groups of C57BL/6 mice were given EGCG (25, 50, or 75 mg/kg body 
      weight) from postnatal day 3 (P3) to P21 and were subjected to sevoflurane (3%; 6 
      h) exposure on P7. EGCG significantly inhibited sevoflurane-induced 
      neuroapoptosis as determined by Fluoro-Jade B staining and terminal 
      deoxynucleotidyl transferase dUTP nick end labelling (TUNEL). Increased levels of 
      cleaved caspase-3, downregulated Bad and Bax, and significantly enhanced Bcl-2, 
      Bcl-xL, xIAP, c-IAP-1, and survivin expression were observed. EGCG induced 
      activation of the PI3K/Akt pathway as evidenced by increased Akt, phospho-Akt, 
      GSK-3beta, phospho-GSK-3beta, and mTORc1 levels. Sevoflurane-mediated downregulation of 
      cAMP/CREB and BDNF/TrkB signalling was inhibited by EGCG. Reverse transcription 
      PCR analysis revealed enhanced BDNF and TrkB mRNA levels upon EGCG 
      administration. Improved performance of mice in Morris water maze tests suggested 
      enhanced learning and memory. The study indicates that EGCG was able to 
      effectively inhibit sevoflurane-induced neurodegeneration and improve learning 
      and memory retention of mice via activation of CREB/BDNF/TrkB-PI3K/Akt 
      signalling.
FAU - Ding, Mei-Li
AU  - Ding ML
AD  - a Department of Pediatrics, Shandong Jining No. 1 People's Hospital, Shandong 
      272011, China.
FAU - Ma, Hui
AU  - Ma H
AD  - b Department of Neurosurgery, Shandong Jining No. 1 People's Hospital, Shandong 
      272011, China.
FAU - Man, Yi-Gang
AU  - Man YG
AD  - a Department of Pediatrics, Shandong Jining No. 1 People's Hospital, Shandong 
      272011, China.
FAU - Lv, Hong-Yan
AU  - Lv HY
AD  - a Department of Pediatrics, Shandong Jining No. 1 People's Hospital, Shandong 
      272011, China.
LA  - eng
PT  - Journal Article
DEP - 20170705
PL  - Canada
TA  - Can J Physiol Pharmacol
JT  - Canadian journal of physiology and pharmacology
JID - 0372712
RN  - 0 (Brain-Derived Neurotrophic Factor)
RN  - 0 (Cyclic AMP Response Element-Binding Protein)
RN  - 0 (Methyl Ethers)
RN  - 0 (Neuroprotective Agents)
RN  - 0 (Polyphenols)
RN  - 0 (Tea)
RN  - 38LVP0K73A (Sevoflurane)
RN  - 8R1V1STN48 (Catechin)
RN  - BQM438CTEL (epigallocatechin gallate)
RN  - E0399OZS9N (Cyclic AMP)
RN  - EC 2.7.10.1 (Receptor, trkB)
RN  - EC 2.7.11.1 (Proto-Oncogene Proteins c-akt)
RN  - EC 2.7.11.1 (TOR Serine-Threonine Kinases)
RN  - EC 3.4.22.- (Caspase 3)
SB  - IM
MH  - Animals
MH  - Animals, Newborn
MH  - Apoptosis/drug effects
MH  - Brain-Derived Neurotrophic Factor/metabolism
MH  - Caspase 3/genetics
MH  - Catechin/*analogs & derivatives/pharmacology
MH  - Cell Survival/drug effects
MH  - Cyclic AMP/metabolism
MH  - Cyclic AMP Response Element-Binding Protein/metabolism
MH  - Cytoprotection/drug effects
MH  - Gene Expression Regulation, Enzymologic/drug effects
MH  - Memory/drug effects
MH  - Methyl Ethers/*pharmacology
MH  - Mice
MH  - Mice, Inbred C57BL
MH  - Neurons/*cytology/*drug effects/metabolism
MH  - Neuroprotective Agents/pharmacology
MH  - Phosphatidylinositol 3-Kinases/metabolism
MH  - Polyphenols/*pharmacology
MH  - Proto-Oncogene Proteins c-akt/metabolism
MH  - Receptor, trkB/metabolism
MH  - Sevoflurane
MH  - Signal Transduction/*drug effects
MH  - Spatial Behavior/drug effects
MH  - TOR Serine-Threonine Kinases/metabolism
MH  - Tea/*chemistry
OTO - NOTNLM
OT  - brain-derived neurotrophic factor
OT  - cAMP response element-binding protein
OT  - epigallocatechin-3-gallate
OT  - facteur neurotrophique derive du cerveau
OT  - neurodegeneration
OT  - neurodegenerescence
OT  - phosphatidylinositol 3-kinase signalling
OT  - proteine de liaison d'elements-AMPc repondante
OT  - sevoflurane
OT  - voie de signalisation de la phosphatidylinositol 3-kinase
OT  - epigallocatechine-3-gallate
EDAT- 2017/07/06 06:00
MHDA- 2018/06/15 06:00
CRDT- 2017/07/06 06:00
PHST- 2017/07/06 06:00 [pubmed]
PHST- 2018/06/15 06:00 [medline]
PHST- 2017/07/06 06:00 [entrez]
AID - 10.1139/cjpp-2016-0333 [doi]
PST - ppublish
SO  - Can J Physiol Pharmacol. 2017 Dec;95(12):1396-1405. doi: 10.1139/cjpp-2016-0333. 
      Epub 2017 Jul 5.