PMID- 21554870
OWN - NLM
STAT- MEDLINE
DCOM- 20111006
LR  - 20220318
IS  - 1879-0712 (Electronic)
IS  - 0014-2999 (Linking)
VI  - 664
IP  - 1-3
DP  - 2011 Aug 16
TI  - Cordycepin protects against cerebral ischemia/reperfusion injury in vivo and in 
      vitro.
PG  - 20-8
LID - 10.1016/j.ejphar.2011.04.052 [doi]
AB  - Cordycepin, (3'-deoxyadenosine), a bioactive compound of Cordyceps militaris, has 
      been shown to exhibit many pharmacological actions, such as anti-inflammatory, 
      antioxidative and anticancer activities. Little is known about the 
      neuroprotective action of cordycepin as well as its molecular mechanisms. In this 
      study, cordycepin was investigated for its neuroprotective potential in mice with 
      ischemia following 15 min of the bilateral common carotid artery occlusion and 4h 
      of reperfusion. The effect of cordycepin was also studied in mice brain slices 
      treated with oxygen-glucose deprivation (OGD) injury. Our results showed that 
      cordycepin was able to prevent postischemic neuronal degeneration and brain slice 
      injury. Excitatory amino acids such as glutamate and aspartate in brain 
      homogenized supernatant, which were increased in ischemia/reperfusion group, were 
      detected by high performance liquid chromatography (HPLC). The results showed 
      that cordycepin was able to decrease the extracellular level of glutamate and 
      aspartate significantly. Moreover, cordycepin was able to increase the activity 
      of superoxide dismutase (SOD) and decrease the level of malondialdehyde (MDA), 
      ameliorating the extent of oxidation. Furthermore, matrix 
      metalloproteinase-3(MMP-3), a key enzyme involved in inflammatory reactions, was 
      markedly increased after ischemia reperfusion, whereas cordycepin was able to 
      inhibit its expression obviously. In conclusion, our in vivo and in vitro study 
      showed that cordycepin was able to exert a potent neuroprotective function after 
      cerebral ischemia/reperfusion.
CI  - Copyright (c) 2011 Elsevier B.V. All rights reserved.
FAU - Cheng, Zhenyong
AU  - Cheng Z
AD  - Department of Pharmacology, School of Basic Medical Sciences, Tongji Medical 
      College, Huazhong University of Science and Technology, Wuhan, PR China.
FAU - He, Wei
AU  - He W
FAU - Zhou, Xiaoxia
AU  - Zhou X
FAU - Lv, Qing
AU  - Lv Q
FAU - Xu, Xulin
AU  - Xu X
FAU - Yang, Shanshan
AU  - Yang S
FAU - Zhao, Chenming
AU  - Zhao C
FAU - Guo, Lianjun
AU  - Guo L
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20110501
PL  - Netherlands
TA  - Eur J Pharmacol
JT  - European journal of pharmacology
JID - 1254354
RN  - 0 (Deoxyadenosines)
RN  - 0 (Excitatory Amino Acids)
RN  - 36015-30-2 (Propidium)
RN  - 4Y8F71G49Q (Malondialdehyde)
RN  - EC 1.15.1.1 (Superoxide Dismutase)
RN  - EC 3.4.24.17 (Matrix Metalloproteinase 3)
RN  - GZ8VF4M2J8 (cordycepin)
RN  - IY9XDZ35W2 (Glucose)
RN  - S88TT14065 (Oxygen)
SB  - IM
MH  - Animals
MH  - Brain Ischemia/*physiopathology
MH  - Cell Count
MH  - Deoxyadenosines/*pharmacology
MH  - Excitatory Amino Acids/metabolism
MH  - Glucose/metabolism
MH  - Hippocampus/pathology
MH  - Male
MH  - Malondialdehyde/metabolism
MH  - Matrix Metalloproteinase 3/metabolism
MH  - Mice
MH  - Neurons/drug effects/pathology
MH  - Oxygen/metabolism
MH  - Propidium/metabolism
MH  - Reperfusion Injury/enzymology/metabolism/pathology/*prevention & control
MH  - Superoxide Dismutase/metabolism
EDAT- 2011/05/11 06:00
MHDA- 2011/10/07 06:00
CRDT- 2011/05/11 06:00
PHST- 2010/09/25 00:00 [received]
PHST- 2011/04/12 00:00 [revised]
PHST- 2011/04/18 00:00 [accepted]
PHST- 2011/05/11 06:00 [entrez]
PHST- 2011/05/11 06:00 [pubmed]
PHST- 2011/10/07 06:00 [medline]
AID - S0014-2999(11)00471-7 [pii]
AID - 10.1016/j.ejphar.2011.04.052 [doi]
PST - ppublish
SO  - Eur J Pharmacol. 2011 Aug 16;664(1-3):20-8. doi: 10.1016/j.ejphar.2011.04.052. 
      Epub 2011 May 1.