PMID- 38141801
OWN - NLM
STAT- MEDLINE
DCOM- 20240214
LR  - 20240308
IS  - 1872-6240 (Electronic)
IS  - 0006-8993 (Linking)
VI  - 1826
DP  - 2024 Mar 1
TI  - In vitro ischemic preconditioning mediates the Ca(2+)/CaN/NFAT pathway to protect 
      against oxygen-glucose deprivation-induced cellular damage and inflammatory 
      responses.
PG  - 148736
LID - S0006-8993(23)00507-3 [pii]
LID - 10.1016/j.brainres.2023.148736 [doi]
AB  - Oxygen-glucose deprivation (OGD) is a critical model for studying 
      hypoxic-ischemic cerebrovascular disease in vitro. This paper is to investigate 
      the protection of OGD-induced cellular damage and inflammatory responses by OGD 
      preconditioning in vitro, to provide a theoretical basis for OGD preconditioning 
      to improve the prevention and prognosis of ischemic stroke. OGD or OGD 
      preconditioning model was established by culturing the PC12 cell line in vitro, 
      followed by further adding A23187 (calcium ion carrier) or CsA (calcium ion 
      antagonist). Cell viability was detected by MTT, apoptosis by Hoechst 33,258 
      staining, the levels of TNF-alpha and IL-1beta mRNA by RT-qPCR and ELISA, and the levels 
      of CaN, NFAT, COX-2 by RT-qPCR and Western blot. Cell viability was decreased, 
      and apoptosis, inflammatory cytokines, and CaN, NFAT, and COX-2 levels were 
      notably increased upon OGD, while OGD pretreatment significantly increased cell 
      viability and decreased apoptosis, inflammation, and the Ca2+/CaN/NFAT pathway. 
      Treatment with A23187 decreased cell viability, promoted apoptosis, and 
      significantly increased TNF-alpha, IL-1beta, CaN, NFAT, and COX-2 levels, while CsA 
      treatment reduced the opposite results. In vitro OGD preconditioning mediates the 
      Ca2+/CaN/NFAT pathway to protect against OGD-induced cellular damage and 
      inflammatory responses.
CI  - Copyright (c) 2023 Elsevier B.V. All rights reserved.
FAU - Zhang, Lihong
AU  - Zhang L
AD  - Department of Neurointervention and Neurocritical Care, Dalian Central Hospital, 
      Affiliated to Dalian University of Technology, Dalian, China; Department of 
      Neurology, The Second Hospital of Dalian Medical University, No. 467 Zhongshan 
      Road, Shahekou District, Dalian 116023, Liaoning, China.
FAU - Guo, Qingzi
AU  - Guo Q
AD  - Deprtment of Cardiothoracic Surgery, Royal Stoke University Hospital, 
      Stoke-on-Trent ST4 6QG, UK.
FAU - An, Ran
AU  - An R
AD  - Department of Neurology, Taihe Hospital, Shiyan 442099, Hubei, China.
FAU - Shen, Shuhan
AU  - Shen S
AD  - Department of Emergency Internal Medicine, The First Affiliated Hospital of 
      Jinzhou Medical University, Jinzhou 121012, Liaoning, China.
FAU - Yin, Lin
AU  - Yin L
AD  - Department of Neurology, The Second Hospital of Dalian Medical University, No. 
      467 Zhongshan Road, Shahekou District, Dalian 116023, Liaoning, China. Electronic 
      address: yinlinn0603@163.com.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20231221
PL  - Netherlands
TA  - Brain Res
JT  - Brain research
JID - 0045503
RN  - S88TT14065 (Oxygen)
RN  - SY7Q814VUP (Calcium)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - IY9XDZ35W2 (Glucose)
RN  - 37H9VM9WZL (Calcimycin)
RN  - EC 1.14.99.1 (Cyclooxygenase 2)
SB  - IM
MH  - Rats
MH  - Animals
MH  - *Oxygen/metabolism
MH  - Calcium
MH  - Tumor Necrosis Factor-alpha
MH  - Glucose
MH  - Calcimycin
MH  - Cyclooxygenase 2
MH  - Apoptosis
MH  - PC12 Cells
MH  - *Ischemic Preconditioning
MH  - Cell Survival
OTO - NOTNLM
OT  - Apoptosis
OT  - Ca2+/CaN/NFAT pathway
OT  - Cell viability
OT  - Inflammatory factors
OT  - Oxygen-glucose deprivation
OT  - Oxygen-glucose deprivation preconditioning
COIS- Declaration of competing interest The authors declare that they have no known 
      competing financial interests or personal relationships that could have appeared 
      to influence the work reported in this paper.
EDAT- 2023/12/24 09:42
MHDA- 2024/02/12 05:43
CRDT- 2023/12/23 19:26
PHST- 2023/11/06 00:00 [received]
PHST- 2023/12/17 00:00 [revised]
PHST- 2023/12/18 00:00 [accepted]
PHST- 2024/02/12 05:43 [medline]
PHST- 2023/12/24 09:42 [pubmed]
PHST- 2023/12/23 19:26 [entrez]
AID - S0006-8993(23)00507-3 [pii]
AID - 10.1016/j.brainres.2023.148736 [doi]
PST - ppublish
SO  - Brain Res. 2024 Mar 1;1826:148736. doi: 10.1016/j.brainres.2023.148736. Epub 2023 
      Dec 21.