PMID- 25271424
OWN - NLM
STAT- MEDLINE
DCOM- 20150610
LR  - 20211021
IS  - 1420-3049 (Electronic)
IS  - 1420-3049 (Linking)
VI  - 19
IP  - 10
DP  - 2014 Sep 30
TI  - Pinocembrin protects the brain against ischemia-reperfusion injury and reverses 
      the autophagy dysfunction in the penumbra area.
PG  - 15786-98
LID - 10.3390/molecules191015786 [doi]
AB  - The aim of this study was to investigate the effects of pinocembrin on brain 
      ischemia/reperfusion (I/R) injury and the potential involvement of autophagy 
      activity changes in the penumbra area in the mechanisms of pinocembrin activity. 
      Focal cerebral I/R model was induced by middle cerebral artery occlusion (MCAO) 
      for 2 h followed by 24 h reperfusion. Pinocembrin was administered intravenously 
      at different doses (1, 3, and 10 mg/kg, respectively) at the onset of 
      reperfusion. Neurological function, brain infarction and brain swelling ratio 
      were evaluated. Terminal deoxynucleotidyl transferase-mediated dUTP nick end 
      labeling (TUNEL) method and immunohistochemical analysis (Caspase-3) were used to 
      evaluate apoptosis in the penumbra cortex. Two key proteins of autophagy, LC3B 
      and Beclin1, were detected by western blot. The results showed that 
      pinocembrin-treatment could significantly reduce neurological deficit scores, 
      infarct volume, cerebral edema and improve pathological lesion in the I/R rats. 
      Pinocembrin-treatment could also reduce the number of TUNEL-positive and 
      Caspase-3-positive neurons, and upregulate the expression of LC3B and Beclin1 in 
      penumbra area. These results suggested that pinocembrin could protect the brain 
      against I/R injury, and the possible mechanisms might be attributed to inhibition 
      of apoptosis and reversed autophagy activity in penumbra area.
FAU - Zhao, Gang
AU  - Zhao G
AD  - Beijing Key Laboratory of Drug Targets Identification and Drug Screening, 
      Institute of Materia Medica, Chinese Academy of Medical Sciences and Peking Union 
      Medical College, Beijing 100050, China. zhiweinuobeier@163.com.
FAU - Zhang, Wen
AU  - Zhang W
AD  - Beijing Key Laboratory of Drug Targets Identification and Drug Screening, 
      Institute of Materia Medica, Chinese Academy of Medical Sciences and Peking Union 
      Medical College, Beijing 100050, China. zhangwen9010@imm.ac.cn.
FAU - Li, Li
AU  - Li L
AD  - Beijing Key Laboratory of Drug Targets Identification and Drug Screening, 
      Institute of Materia Medica, Chinese Academy of Medical Sciences and Peking Union 
      Medical College, Beijing 100050, China. lili@imm.ac.cn.
FAU - Wu, Song
AU  - Wu S
AD  - Beijing Key Laboratory of Drug Targets Identification and Drug Screening, 
      Institute of Materia Medica, Chinese Academy of Medical Sciences and Peking Union 
      Medical College, Beijing 100050, China. ws@imm.ac.cn.
FAU - Du, Guanhua
AU  - Du G
AD  - Beijing Key Laboratory of Drug Targets Identification and Drug Screening, 
      Institute of Materia Medica, Chinese Academy of Medical Sciences and Peking Union 
      Medical College, Beijing 100050, China. dugh@imm.ac.cn.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20140930
PL  - Switzerland
TA  - Molecules
JT  - Molecules (Basel, Switzerland)
JID - 100964009
RN  - 0 (Flavanones)
RN  - 0 (Neuroprotective Agents)
RN  - 8T7C8CH791 (pinocembrin)
RN  - EC 3.4.22.- (Caspase 3)
SB  - IM
MH  - Animals
MH  - Autophagy/*drug effects
MH  - Brain Edema/drug therapy/etiology
MH  - Brain Infarction/drug therapy/pathology
MH  - Brain Ischemia/drug therapy/metabolism/pathology/physiopathology
MH  - Caspase 3/metabolism
MH  - Disease Models, Animal
MH  - Flavanones/administration & dosage/*pharmacology
MH  - Male
MH  - Neuroprotective Agents/administration & dosage/*pharmacology
MH  - Rats
MH  - Reperfusion Injury/drug therapy/*metabolism/*pathology
PMC - PMC6271208
COIS- The authors declare no conflict of interest.
EDAT- 2014/10/02 06:00
MHDA- 2015/06/11 06:00
PMCR- 2014/09/30
CRDT- 2014/10/02 06:00
PHST- 2014/07/31 00:00 [received]
PHST- 2014/09/06 00:00 [revised]
PHST- 2014/09/15 00:00 [accepted]
PHST- 2014/10/02 06:00 [entrez]
PHST- 2014/10/02 06:00 [pubmed]
PHST- 2015/06/11 06:00 [medline]
PHST- 2014/09/30 00:00 [pmc-release]
AID - molecules191015786 [pii]
AID - molecules-19-15786 [pii]
AID - 10.3390/molecules191015786 [doi]
PST - epublish
SO  - Molecules. 2014 Sep 30;19(10):15786-98. doi: 10.3390/molecules191015786.