PMID- 28552673
OWN - NLM
STAT- MEDLINE
DCOM- 20180209
LR  - 20180317
IS  - 1873-2747 (Electronic)
IS  - 0361-9230 (Linking)
VI  - 132
DP  - 2017 Jun
TI  - Neuroprotective effects of sulfiredoxin-1 during cerebral ischemia/reperfusion 
      oxidative stress injury in rats.
PG  - 99-108
LID - S0361-9230(17)30060-6 [pii]
LID - 10.1016/j.brainresbull.2017.05.012 [doi]
AB  - As an endogenous antioxidant protein, Sulfiredoxin1 (Srxn1) can prevent cell 
      oxidative stress damage. However, its role in cerebral ischemia/reperfusion (I/R) 
      injury and the underlying signaling mechanisms remain largely unknown. Here, we 
      explored effects of Srxn1 knockdown on oxidative stress using in vitro and in 
      vivo I/R models and investigated related neuroprotective mechanisms. For in vitro 
      studies, primary cortical neuronal cultures were transfected with an interfering 
      lentivirus targeting Srxn1. Oxygen-glucose deprivation (OGD) was conducted after 
      Srxn1 knockdown. MTS and lactate dehydrogenase assays indicated that knockdown of 
      Srxn1 increased cell death and reduced cell viability. Similarly, superoxide 
      dismutase (SOD) and reduced glutathionekits assays showed that knockdown of Srxn1 
      worsened oxidative stress injury. For in vivo studies, siRNA for Srxn1 or 
      negative control siRNA was injected intracerebroventricularly 24h before middle 
      cerebral artery occlusion (MCAO). Data shows silencing Srxn1 resulted in a 
      significant increase in cerebral infarction, neurological deficits, histological 
      injury, and oxidative stress injury 24h after ischemic stroke. Moreover, 
      immunoblot analysis assessed the relationship between Srxn1 levels and Prdx1-4 as 
      well as Prdx-SO3 activity both in vitro and in vivo models. We found that 
      decreased Srxn1 reduced Prdx1-4 and enhanced Prdx-SO3 protein levels. In 
      addition, knockdown of Nrf2 was performed; immunoblot analysis was used to 
      measure Srxn1 and NQO1 protein levels. We further found that interference of Nrf2 
      reduced Srxn1 and NQO1 protein levels. In summary, Srxn1 can protect neurons from 
      I/R oxidative stress injury and the mechanism involves Prdx activity. Srxn1, 
      which might be downstream of Nrf2, can prevent cerebral ischemia reperfusion by 
      reversing overoxidized Prdx and restoring antioxidant activity of Prdx.
CI  - Copyright (c) 2017. Published by Elsevier Inc.
FAU - Wu, Jingxian
AU  - Wu J
AD  - Department of Pathology, Chongqing Medical University, Chongqing 400016, PR 
      China.
FAU - Chen, Yanlin
AU  - Chen Y
AD  - Department of Pathology, Chongqing Medical University, Chongqing 400016, PR 
      China; The First Affiliated Hospital of Chongqing Medical University, Chongqing 
      400016, PR China.
FAU - Yu, Shanshan
AU  - Yu S
AD  - Department of Pathology, Chongqing Medical University, Chongqing 400016, PR 
      China.
FAU - Li, Lingyu
AU  - Li L
AD  - Department of Pathology, Chongqing Medical University, Chongqing 400016, PR 
      China.
FAU - Zhao, Xiujuan
AU  - Zhao X
AD  - Neurology Center, University-Town Hospital of Chongqing Medical University, 
      Chongqing 401331, PR China.
FAU - Li, Qiong
AU  - Li Q
AD  - Department of Pathology, Chongqing Medical University, Chongqing 400016, PR 
      China; Department of Pathology, Shapingba District People's Hospital, Chongqing 
      400030, PR China.
FAU - Zhao, Jing
AU  - Zhao J
AD  - Department of Pathophysiology, Chongqing Medical University, Chongqing 400016, PR 
      China.
FAU - Zhao, Yong
AU  - Zhao Y
AD  - Department of Pathology, Chongqing Medical University, Chongqing 400016, PR 
      China. Electronic address: zhaoyong668@cqmu.edu.cn.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20170524
PL  - United States
TA  - Brain Res Bull
JT  - Brain research bulletin
JID - 7605818
RN  - 0 (RNA, Small Interfering)
RN  - EC 1.11.1.15 (Peroxiredoxins)
RN  - EC 1.8.- (Oxidoreductases Acting on Sulfur Group Donors)
RN  - EC 1.8.- (Srxn1 protein, rat)
RN  - IY9XDZ35W2 (Glucose)
SB  - IM
MH  - Animals
MH  - Brain/metabolism/pathology
MH  - Brain Infarction/metabolism/pathology
MH  - Brain Ischemia/*metabolism/pathology
MH  - Cell Death/physiology
MH  - Cell Hypoxia/*physiology
MH  - Cell Survival/physiology
MH  - Cells, Cultured
MH  - Disease Models, Animal
MH  - Glucose/deficiency
MH  - Male
MH  - Neurons/metabolism/pathology
MH  - Neuroprotection/*physiology
MH  - Oxidative Stress/physiology
MH  - Oxidoreductases Acting on Sulfur Group Donors/administration & 
      dosage/genetics/*metabolism
MH  - Peroxiredoxins/metabolism
MH  - RNA, Small Interfering
MH  - Rats, Sprague-Dawley
MH  - Reperfusion Injury/*metabolism/pathology
MH  - Stroke/*metabolism/pathology
OTO - NOTNLM
OT  - Ischemia/reperfusion
OT  - Neuroprotection
OT  - Oxidative stress
OT  - Peroxiredoxin
OT  - Sulfiredoxin1
EDAT- 2017/05/30 06:00
MHDA- 2018/02/10 06:00
CRDT- 2017/05/30 06:00
PHST- 2017/02/04 00:00 [received]
PHST- 2017/05/12 00:00 [revised]
PHST- 2017/05/22 00:00 [accepted]
PHST- 2017/05/30 06:00 [pubmed]
PHST- 2018/02/10 06:00 [medline]
PHST- 2017/05/30 06:00 [entrez]
AID - S0361-9230(17)30060-6 [pii]
AID - 10.1016/j.brainresbull.2017.05.012 [doi]
PST - ppublish
SO  - Brain Res Bull. 2017 Jun;132:99-108. doi: 10.1016/j.brainresbull.2017.05.012. 
      Epub 2017 May 24.