PMID- 24096211
OWN - NLM
STAT- MEDLINE
DCOM- 20140620
LR  - 20131104
IS  - 1872-6240 (Electronic)
IS  - 0006-8993 (Linking)
VI  - 1538
DP  - 2013 Nov 13
TI  - Sodium hydrosulfide prevents hypoxia-induced behavioral impairment in neonatal 
      mice.
PG  - 126-34
LID - S0006-8993(13)01317-6 [pii]
LID - 10.1016/j.brainres.2013.09.043 [doi]
AB  - Hypoxic encephalopathy is a common cause of neonatal seizures and long-term 
      neurological abnormalities. Endogenous hydrogen sulfide (H2S) may have multiple 
      functions in brain. The aim of this study is to investigate whether sodium 
      hydrosulfide (NaHS), a H2S donor, provides protection against neonatal 
      hypoxia-induced neurobehavioral deficits. Neonatal mice were subjected to hypoxia 
      (5% oxygen for 120min) at postnatal day 1 and received NaHS (5.6mg/kg) once daily 
      for 3d. Neurobehavioral toxicity was examined at 3-30d after hypoxia. Treatment 
      with NaHS significantly attenuated the delayed development of sensory and motor 
      reflexes induced by hypoxia up to two weeks after the insult. Moreover, NaHS 
      improved the learning and memory performance of hypoxic animals as indicated in 
      Morris water maze test at 30d after hypoxia. In mice exposed to hypoxia, 
      treatment with NaHS enhanced expression of brain derived neurotrophic factor 
      (BDNF) in the hippocampus. Furthermore, the protective effects of NaHS were 
      associated with its ability to repress the hypoxia-induced nitric oxide synthase 
      (NOS) activity and nitric oxide production in the hippocampus of mice brain. 
      Taken together, these results suggest that the long-lasting beneficial effects of 
      NaHS on hypoxia-induced neurobehavioral deficits are mediated, at least in part, 
      by inducing BDNF expression and suppressing NOS activity in the brain of mice.
CI  - (c) 2013 Elsevier B.V. All rights reserved.
FAU - Wang, Zhen
AU  - Wang Z
AD  - Institution of Physiology, Shandong University School of Medicine, 44# Wenhua Xi 
      Road, Jinan, Shandong 250012, PR China.
FAU - Zhan, Jingmin
AU  - Zhan J
FAU - Wang, Xueer
AU  - Wang X
FAU - Gu, Jianhua
AU  - Gu J
FAU - Xie, Kai
AU  - Xie K
FAU - Zhang, Qingrui
AU  - Zhang Q
FAU - Liu, Dexiang
AU  - Liu D
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20131003
PL  - Netherlands
TA  - Brain Res
JT  - Brain research
JID - 0045503
RN  - 0 (Brain-Derived Neurotrophic Factor)
RN  - 0 (Sulfides)
RN  - 31C4KY9ESH (Nitric Oxide)
RN  - EC 1.14.13.39 (Nitric Oxide Synthase)
RN  - FWU2KQ177W (sodium bisulfide)
SB  - IM
MH  - Animals
MH  - Animals, Newborn
MH  - Behavior, Animal
MH  - Brain-Derived Neurotrophic Factor/metabolism
MH  - Female
MH  - Hippocampus/metabolism
MH  - Hypoxia, Brain/*drug therapy/metabolism/physiopathology
MH  - Male
MH  - Maze Learning/physiology
MH  - Memory Disorders/*etiology/metabolism/physiopathology
MH  - Mice
MH  - Mice, Inbred BALB C
MH  - Nitric Oxide/metabolism
MH  - Nitric Oxide Synthase/metabolism
MH  - Sulfides/*therapeutic use
OTO - NOTNLM
OT  - Brain derived neurotrophic factor
OT  - Hypoxia
OT  - Nitric oxide
OT  - Sodium hydrosulfide
EDAT- 2013/10/08 06:00
MHDA- 2014/06/21 06:00
CRDT- 2013/10/08 06:00
PHST- 2013/06/06 00:00 [received]
PHST- 2013/09/18 00:00 [revised]
PHST- 2013/09/26 00:00 [accepted]
PHST- 2013/10/08 06:00 [entrez]
PHST- 2013/10/08 06:00 [pubmed]
PHST- 2014/06/21 06:00 [medline]
AID - S0006-8993(13)01317-6 [pii]
AID - 10.1016/j.brainres.2013.09.043 [doi]
PST - ppublish
SO  - Brain Res. 2013 Nov 13;1538:126-34. doi: 10.1016/j.brainres.2013.09.043. Epub 
      2013 Oct 3.