PMID- 30784940
OWN - NLM
STAT- MEDLINE
DCOM- 20190808
LR  - 20190808
IS  - 1950-6007 (Electronic)
IS  - 0753-3322 (Linking)
VI  - 112
DP  - 2019 Apr
TI  - Hyperglycemia aggravates spinal cord injury through endoplasmic reticulum stress 
      mediated neuronal apoptosis, gliosis and activation.
PG  - 108672
LID - S0753-3322(18)33858-7 [pii]
LID - 10.1016/j.biopha.2019.108672 [doi]
AB  - BACKGROUND: Hyperglycemia has been shown to influence prognostic outcome of 
      spinal cord injury (SCI). However, the corresponding mechanism is not very clear. 
      AIM: This study is expected to explore the role of endoplasmic reticulum (ER) 
      stress in hyperglycemia aggravated SCI. METHODS: Hyperglycemia was established in 
      rats by intraperitoneal (i.p.) injection of streptozotocin. SCI was performed at 
      the T10 of spinal cord through weight dropping. ER stress was suppressed by oral 
      gavage of 4-PBA. ER stress, histological change of the injured spinal cords, 
      neuronal apoptosis, demyelination, glial proliferation, inflammatory factor 
      production, blood-spinal cord barrier (BSCB) permeability, TJ (Occludin, 
      Claudin5) and AJ (beta-catenin, P120) protein degradation, and locomotor recovery 
      were determined using western blotting, immunohistochemistry, HE staining, Evan's 
      Blue assay, BBB scores and inclined plane test, respectively. In vitro, rat 
      spinal cord neurons cells (RSCNCs) and cerebral microvascular endothelial cells 
      (RCMECs) were stimulated with high glucose (HG) and/or thapsigargin (TG). The 
      effects of HG and/or TG on RSCNCs apoptosis, and AJ and TJ expression by RCMECs 
      were evaluated with flow cytometry and western blotting, respectively. RESULTS: 
      Hyperglycemic rats exhibited enhanced ER stress, increased neuronal apoptosis, 
      aggravated demyelination, increased glial proliferation and inflammatory factors 
      secretion, more serious BSCB disruption and disturbed locomotor recovery. ER 
      stress inhibition alleviated hyperglycemia induced adverse effect on neuronal 
      apoptosis and BSCB permeability, whereas showed little influence on glial 
      activation and inflammation. CONCLUSION: ER stress was aggravated in 
      hyperglycemic rats after SCI, and subsequently promoted neuronal apoptosis and 
      BSCB disruption in rats.
CI  - Copyright (c) 2019 Elsevier Masson SAS. All rights reserved.
FAU - Chen, Zhirong
AU  - Chen Z
AD  - Department of Orthopedics, General Hospital of Ningxia Medical University, 
      Yinchuan, 750004, Ningxia, China.
FAU - Guo, Haohui
AU  - Guo H
AD  - Department of Orthopedics, General Hospital of Ningxia Medical University, 
      Yinchuan, 750004, Ningxia, China.
FAU - Lu, Zhidong
AU  - Lu Z
AD  - Department of Orthopedics, General Hospital of Ningxia Medical University, 
      Yinchuan, 750004, Ningxia, China.
FAU - Sun, Kening
AU  - Sun K
AD  - Department of Orthopedics, General Hospital of Ningxia Medical University, 
      Yinchuan, 750004, Ningxia, China.
FAU - Jin, Qunhua
AU  - Jin Q
AD  - Department of Orthopedics, General Hospital of Ningxia Medical University, 
      Yinchuan, 750004, Ningxia, China. Electronic address: jinqunhua@sina.com.
LA  - eng
PT  - Journal Article
DEP - 20190218
PL  - France
TA  - Biomed Pharmacother
JT  - Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie
JID - 8213295
MH  - Animals
MH  - Apoptosis/*physiology
MH  - Cells, Cultured
MH  - Endoplasmic Reticulum Stress/*physiology
MH  - Gliosis/etiology/*metabolism/pathology
MH  - Hyperglycemia/complications/*metabolism/pathology
MH  - Random Allocation
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - Spinal Cord Injuries/*metabolism/pathology
OTO - NOTNLM
OT  - Endoplasmic reticulum (ER) stress
OT  - Glial proliferation
OT  - Hyperglycemia
OT  - Neuronal apoptosis
OT  - Spinal cord injury (SCI)
EDAT- 2019/02/21 06:00
MHDA- 2019/08/09 06:00
CRDT- 2019/02/21 06:00
PHST- 2018/06/06 00:00 [received]
PHST- 2019/01/29 00:00 [revised]
PHST- 2019/02/05 00:00 [accepted]
PHST- 2019/02/21 06:00 [pubmed]
PHST- 2019/08/09 06:00 [medline]
PHST- 2019/02/21 06:00 [entrez]
AID - S0753-3322(18)33858-7 [pii]
AID - 10.1016/j.biopha.2019.108672 [doi]
PST - ppublish
SO  - Biomed Pharmacother. 2019 Apr;112:108672. doi: 10.1016/j.biopha.2019.108672. Epub 
      2019 Feb 18.