PMID- 24277159
OWN - NLM
STAT- MEDLINE
DCOM- 20150106
LR  - 20211021
IS  - 1476-3524 (Electronic)
IS  - 1029-8428 (Linking)
VI  - 26
IP  - 1
DP  - 2014 Jul
TI  - (S)-ZJM-289 preconditioning induces a late phase protection against nervous 
      injury induced by transient cerebral ischemia and oxygen-glucose deprivation.
PG  - 16-31
LID - 10.1007/s12640-013-9444-x [doi]
AB  - (S)-ZJM-289, a novel nitric oxide (NO)-releasing derivative of 
      3-n-butylphthalide, induces the neuroprotection in a rat model of focal cerebral 
      ischemia/reperfusion (I/R). However, much is unknown about the late phase effect 
      in the neuroprotection of (S)-ZJM-289 preconditioning. The purpose of this study 
      is to explore the late phase neuroprotection of (S)-ZJM-289 preconditioning, as 
      well as underlying mechanisms involved. Preconditioning with 40-160 mg/kg, 
      (S)-ZJM-289 significantly reduces brain damage after I/R. (S)-ZJM-289 
      preconditioning is effective when applied 1-3 days before I/R. Moreover, the 
      degrees of neuroprotection offered by (S)-ZJM-289 preconditioning and ischemic 
      preconditioning are virtually identical. (S)-ZJM-289 preconditioning also 
      protects primary cultured cortical neurons against oxygen-glucose deprivation and 
      recovery-induced cytotoxicity in vitro. (S)-ZJM-289 preconditioning significantly 
      increases the generation of NO, but has no effect on the nitric oxide synthase 
      activities. Additionally, (S)-ZJM-289 preconditioning promotes the dissociation 
      between nuclear-factor-E2-related factor (Nrf2) and kelch-like ECH-associated 
      protein 1, and induces Nrf2 nuclear localization. The neuroprotection of 
      (S)-ZJM-289 preconditioning is blocked by Nrf2-siRNA in vitro. (S)-ZJM-289 
      preconditioning up-regulates antioxidant enzymes against nervous injury. 
      (S)-ZJM-289 preconditioning significantly activates extracellular regulated 
      protein kinases (ERK) and inhibits c-Jun N-terminal kinases signaling cascade. 
      The neuroprotection is abolished by the ERK inhibitor PD98059 in vitro. 
      Subsequently, (S)-ZJM-289 preconditioning increases the levels of anti-apoptotic 
      protein B cell lymphoma 2 (Bcl-2) and inhibited the translocation of Bcl-2 
      associated X to the mitochondria, thus attenuating the release of cytochrome c 
      from the mitochondria and the activation of downstream caspase. These results 
      suggest that (S)-ZJM-289 preconditioning exerts the late phase protection against 
      nervous injury induced by transient cerebral ischemia and oxygen-glucose 
      deprivation.
FAU - Zhang, Chao
AU  - Zhang C
AD  - State Key Laboratory of Natural Medicines, China Pharmaceutical University, 
      Nanjing, 210009, People's Republic of China.
FAU - Zhang, Zhenzhen
AU  - Zhang Z
FAU - Zhao, Qian
AU  - Zhao Q
FAU - Wang, Xuliang
AU  - Wang X
FAU - Ji, Hui
AU  - Ji H
FAU - Zhang, Yihua
AU  - Zhang Y
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20131126
PL  - United States
TA  - Neurotox Res
JT  - Neurotoxicity research
JID - 100929017
RN  - 0 ((2-(1-diethylaminoacetoxy)pentyl)benzoic acid 
      (2-methoxy-4-(2-(4-nitrooxybutoxycarbonyl)vinyl))phenyl ester)
RN  - 0 (Cinnamates)
RN  - 0 (Flavonoids)
RN  - 0 (Neuroprotective Agents)
RN  - 0 (Nitrates)
RN  - 0 (Protein Kinase Inhibitors)
RN  - 31C4KY9ESH (Nitric Oxide)
RN  - EC 1.14.13.39 (Nitric Oxide Synthase)
RN  - IY9XDZ35W2 (Glucose)
RN  - SJE1IO5E3I (2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one)
SB  - IM
MH  - Animals
MH  - Apoptosis/drug effects/physiology
MH  - Brain/drug effects/physiopathology
MH  - Cells, Cultured
MH  - Cinnamates/chemistry/*pharmacology
MH  - Flavonoids/pharmacology
MH  - Glucose/*deficiency
MH  - Hypoxia-Ischemia, Brain/*drug therapy/physiopathology
MH  - Infarction, Middle Cerebral Artery/drug therapy/physiopathology
MH  - Ischemic Attack, Transient/*drug therapy/physiopathology
MH  - MAP Kinase Signaling System/drug effects
MH  - Male
MH  - Mitochondria/drug effects/physiology
MH  - Neurons/*drug effects/physiology
MH  - Neuroprotective Agents/chemistry/*pharmacology
MH  - Nitrates/chemistry/*pharmacology
MH  - Nitric Oxide/metabolism
MH  - Nitric Oxide Synthase/metabolism
MH  - Protein Kinase Inhibitors/pharmacology
MH  - Rats, Sprague-Dawley
EDAT- 2013/11/28 06:00
MHDA- 2015/01/07 06:00
CRDT- 2013/11/27 06:00
PHST- 2013/07/05 00:00 [received]
PHST- 2013/11/15 00:00 [accepted]
PHST- 2013/11/11 00:00 [revised]
PHST- 2013/11/27 06:00 [entrez]
PHST- 2013/11/28 06:00 [pubmed]
PHST- 2015/01/07 06:00 [medline]
AID - 10.1007/s12640-013-9444-x [doi]
PST - ppublish
SO  - Neurotox Res. 2014 Jul;26(1):16-31. doi: 10.1007/s12640-013-9444-x. Epub 2013 Nov 
      26.