PMID- 24907941
OWN - NLM
STAT- MEDLINE
DCOM- 20150714
LR  - 20221207
IS  - 1559-1166 (Electronic)
IS  - 0895-8696 (Linking)
VI  - 54
IP  - 3
DP  - 2014 Nov
TI  - PACAP38 suppresses cortical damage in mice with traumatic brain injury by 
      enhancing antioxidant activity.
PG  - 370-9
LID - 10.1007/s12031-014-0309-4 [doi]
AB  - The production of reactive oxygen species (ROS) and the resulting oxidative 
      stress in mice in response to a controlled cortical impact (CCI) are typical 
      exacerbating factors associated with traumatic brain injury (TBI). Pituitary 
      adenylate cyclase-activating polypeptide 38 (PACAP38) is a multifunctional 
      peptide that has been shown to exhibit neuroprotective effects in response to a 
      diverse range of injuries to neuronal cells. We recently reported that PACAP38 
      might regulate oxidative stress in mice. The aim of the present study was to 
      determine whether PACAP38 exerts neuroprotective effects by regulating oxidative 
      stress in mice with TBI. Reactive oxidative metabolites (ROMs) and biological 
      antioxidant potential (BAP) were measured in male C57Bl/6 mice before and 3, 4, 
      and 24 h after CCI. PACAP38 was administered intravenously immediately following 
      CCI, and immunostaining for the oxidative stress indicator nitrotyrosine (NT), 
      and for neuronal death as an indicator of the area affected by TBI, was measured 
      24 h later. Western blot experiments to determine antioxidant activity [as 
      indicated by superoxide dismutase-2 (SOD-2) and glutathione peroxidase 1 (GPx-1)] 
      in the neocortical region were also performed 3 h post-CCI. Results showed that 
      plasma BAP and ROM levels were dramatically increased 3 h after CCI. PACAP38 
      suppressed the extent of TBI and NT-positive regions 24 h after CCI, and 
      increased SOD-2 and GPx-1 levels in both hemispheres. Taken together, these 
      results suggest that increasing antioxidant might be involving in the 
      neuroprotective effect of PACAP38 in mice subjected to a CCI.
FAU - Miyamoto, Kazuyuki
AU  - Miyamoto K
AD  - Department of Anatomy, Showa University School of Medicine, 1-5-8 Hatanodai, 
      Shinagawa-ku, Tokyo, 142-8555, Japan.
FAU - Tsumuraya, Tomomi
AU  - Tsumuraya T
FAU - Ohtaki, Hirokazu
AU  - Ohtaki H
FAU - Dohi, Kenji
AU  - Dohi K
FAU - Satoh, Kazue
AU  - Satoh K
FAU - Xu, Zhifang
AU  - Xu Z
FAU - Tanaka, Sachiko
AU  - Tanaka S
FAU - Murai, Norimitsu
AU  - Murai N
FAU - Watanabe, Jun
AU  - Watanabe J
FAU - Sugiyama, Koichi
AU  - Sugiyama K
FAU - Aruga, Tohru
AU  - Aruga T
FAU - Shioda, Seiji
AU  - Shioda S
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20140608
PL  - United States
TA  - J Mol Neurosci
JT  - Journal of molecular neuroscience : MN
JID - 9002991
RN  - 0 (Pituitary Adenylate Cyclase-Activating Polypeptide)
RN  - 0 (Reactive Oxygen Species)
RN  - EC 1.11.1.9 (Glutathione Peroxidase)
RN  - EC 1.15.1.1 (Superoxide Dismutase)
RN  - EC 1.15.1.1 (superoxide dismutase 2)
RN  - EC 1.11.1.9 (Glutathione Peroxidase GPX1)
RN  - EC 1.11.1.9 (Gpx1 protein, mouse)
SB  - IM
MH  - Animals
MH  - Brain Injuries/drug therapy/*metabolism
MH  - Glutathione Peroxidase/*metabolism
MH  - Male
MH  - Mice
MH  - Mice, Inbred C57BL
MH  - Neocortex/drug effects/*metabolism
MH  - Oxidative Stress
MH  - Pituitary Adenylate Cyclase-Activating Polypeptide/*pharmacology/therapeutic use
MH  - Reactive Oxygen Species/metabolism
MH  - Superoxide Dismutase/*metabolism
MH  - Glutathione Peroxidase GPX1
EDAT- 2014/06/09 06:00
MHDA- 2015/07/15 06:00
CRDT- 2014/06/09 06:00
PHST- 2014/02/26 00:00 [received]
PHST- 2014/04/14 00:00 [accepted]
PHST- 2014/06/09 06:00 [entrez]
PHST- 2014/06/09 06:00 [pubmed]
PHST- 2015/07/15 06:00 [medline]
AID - 10.1007/s12031-014-0309-4 [doi]
PST - ppublish
SO  - J Mol Neurosci. 2014 Nov;54(3):370-9. doi: 10.1007/s12031-014-0309-4. Epub 2014 
      Jun 8.