PMID- 29334839
OWN - NLM
STAT- MEDLINE
DCOM- 20180820
LR  - 20211204
IS  - 1743-1328 (Electronic)
IS  - 0161-6412 (Linking)
VI  - 40
IP  - 3
DP  - 2018 Mar
TI  - Bax inhibitor-1 is required for resisting the Early Brain Injury induced by 
      subarachnoid hemorrhage through regulating IRE1-JNK pathway.
PG  - 189-196
LID - 10.1080/01616412.2018.1424699 [doi]
AB  - Background and Purpose Bax inhibitor-1 (BI-1) has been identified as a suppressor 
      of Bax-mediated cell apoptosis by regulation of endoplasmic reticulum 
      stress-induced cell death. However, the role of BI-1 in Early Brain Injury (EBI) 
      after subarachnoid hemorrhage (SAH) remains unclear. In the present study, we aim 
      to explore the neuroprotective functions of BI-1 in EBI after SAH by using models 
      of SAH that induced endovascular perforation in rats. Method The neurological 
      score, brain water content and blood-brain barrier (BBB) permeability were 
      evaluated simultaneously as prognostic indicators. Western blot, RT-PCR and TUNEL 
      staining were performed to study the role and mechanisms of BI-1 in EBI after 
      SAH. Results We found that BI-1 knockdown increased histological injury and the 
      percentages of TUNEL-positive neuron in hippocampal, promoted the expressions of 
      endoplasmic reticulum (ER) stress proteins inositol-requiring enzyme 1alpha (IRE1alpha) 
      and TNF receptor-associated factor 2 (TRAF2), and increased the activation levels 
      of apoptosis signal-regulating kinase 1 (ASK1) and c-Jun N-terminal kinase (JNK) 
      in the hippocampus of SAH rats compared with rats in SAH + vehicle group. 
      Conclusion Our results indicate that BI-1 may participate in the regulation of 
      EBI after SAH by regulating IRE1-JNK pathway. Thus, the results suggest that BI-1 
      may be a potential therapeutic target for SAH treatment.
FAU - Shi, Lei
AU  - Shi L
AD  - a Department of Neurosurgery , Zhumadian Central Hospital , Zhumadian , China.
FAU - Wang, Zaizong
AU  - Wang Z
AD  - a Department of Neurosurgery , Zhumadian Central Hospital , Zhumadian , China.
FAU - Liu, Xianjin
AU  - Liu X
AD  - a Department of Neurosurgery , Zhumadian Central Hospital , Zhumadian , China.
FAU - Li, Mao
AU  - Li M
AD  - a Department of Neurosurgery , Zhumadian Central Hospital , Zhumadian , China.
FAU - Zhang, Shangfei
AU  - Zhang S
AD  - a Department of Neurosurgery , Zhumadian Central Hospital , Zhumadian , China.
FAU - Song, Xiaobin
AU  - Song X
AD  - b Department of Neurosurgery , The First Affiliated Hospital of Kunming Medical 
      College , Kunming , China.
LA  - eng
PT  - Journal Article
DEP - 20180116
PL  - England
TA  - Neurol Res
JT  - Neurological research
JID - 7905298
RN  - 0 (Apoptosis Regulatory Proteins)
RN  - 0 (Membrane Proteins)
RN  - 0 (RNA, Messenger)
RN  - 0 (RNA, Small Interfering)
RN  - 0 (Tmbim6 protein, rat)
RN  - EC 2.7.1.- (Ern2 protein, rat)
RN  - EC 2.7.11.1 (Protein Serine-Threonine Kinases)
SB  - IM
MH  - Animals
MH  - Apoptosis Regulatory Proteins/genetics/*metabolism
MH  - Brain Edema/etiology
MH  - Brain Injuries/*etiology/mortality/*therapy
MH  - Disease Models, Animal
MH  - Gene Expression Regulation/physiology
MH  - Humans
MH  - In Situ Nick-End Labeling
MH  - MAP Kinase Signaling System/*physiology
MH  - Male
MH  - Membrane Proteins/genetics/*metabolism
MH  - Neurologic Examination
MH  - Protein Serine-Threonine Kinases/genetics/*metabolism
MH  - RNA, Messenger/metabolism
MH  - RNA, Small Interfering/therapeutic use
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - Subarachnoid Hemorrhage/*complications
MH  - Time Factors
OTO - NOTNLM
OT  - Bax inhibitor-1
OT  - Early Brain Injury
OT  - IRE1-JNK pathway
OT  - hippocampus
OT  - subarachnoid hemorrhage
EDAT- 2018/01/18 06:00
MHDA- 2018/08/21 06:00
CRDT- 2018/01/17 06:00
PHST- 2018/01/18 06:00 [pubmed]
PHST- 2018/08/21 06:00 [medline]
PHST- 2018/01/17 06:00 [entrez]
AID - 10.1080/01616412.2018.1424699 [doi]
PST - ppublish
SO  - Neurol Res. 2018 Mar;40(3):189-196. doi: 10.1080/01616412.2018.1424699. Epub 2018 
      Jan 16.