PMID- 27994507
OWN - NLM
STAT- MEDLINE
DCOM- 20171020
LR  - 20181113
IS  - 1449-2288 (Electronic)
IS  - 1449-2288 (Linking)
VI  - 12
IP  - 12
DP  - 2016
TI  - Catalpol Protects Pre-Myelinating Oligodendrocytes against Ischemia-induced 
      Oxidative Injury through ERK1/2 Signaling Pathway.
PG  - 1415-1426
AB  - The vulnerability of pre-myelinating oligodendrocytes (PreOLs) to ischemic injury 
      plays an important role in the pathogenesis and progression of perinatal white 
      matter injury. Although oxidative stress is thought to be a major pathogenic 
      mechanism predisposing the PreOLs to injury, no effective therapies have been 
      identified to date. The present study aimed to investigate the direct protective 
      effects of catalpol, a potent antioxidant and free radical scavenger, on 
      ischemia-induced oxidative damage in PreOLs and to explore whether the ERK1/2 
      signaling pathway contributed to the protection provided by catalpol. Primary 
      cultures of PreOLs exposed to oxygen-glucose deprivation (OGD) followed by 
      reperfusion were used as an in vitro model of ischemia. Pretreatment with 0.5 mM 
      catalpol for 1 h prior to OGD treatment significantly reversed ischemia-induced 
      apoptosis in PreOLs and myelination deficits by inhibiting intracellular Ca(2+) 
      increase, reducing mitochondrial damage, and ameliorating overproduction of 
      reactive oxygen species (ROS). The expression levels of phosphorylated ERK1/2 
      (p-ERK1/2) and activated poly-ADP-ribose polymerase-1 (PARP-1) were also markedly 
      decreased by catalpol treatment. Blocking the ERK1/2 signaling pathway with the 
      MEK inhibitor U0126 and catalpol significantly protected PreOLs from ROS-mediated 
      apoptosis under OGD. Taken together, these results suggest that catalpol protects 
      PreOLs against ischemia-induced oxidative injury through ERK1/2 signaling 
      pathway. Catalpol may be a candidate for treating ischemic white matter damage.
FAU - Cai, Qiyan
AU  - Cai Q
AD  - Chongqing Key Laboratory of Neurobiology, Department of Histology and Embryology, 
      College of Basic Medicine, The Third Military Medical University, Chongqing, 
      China.
FAU - Ma, Teng
AU  - Ma T
AD  - Chongqing Key Laboratory of Neurobiology, Department of Histology and Embryology, 
      College of Basic Medicine, The Third Military Medical University, Chongqing, 
      China.
FAU - Li, Chengren
AU  - Li C
AD  - Chongqing Key Laboratory of Neurobiology, Department of Histology and Embryology, 
      College of Basic Medicine, The Third Military Medical University, Chongqing, 
      China.
FAU - Tian, Yanping
AU  - Tian Y
AD  - Chongqing Key Laboratory of Neurobiology, Department of Histology and Embryology, 
      College of Basic Medicine, The Third Military Medical University, Chongqing, 
      China.
FAU - Li, Hongli
AU  - Li H
AD  - Chongqing Key Laboratory of Neurobiology, Department of Histology and Embryology, 
      College of Basic Medicine, The Third Military Medical University, Chongqing, 
      China.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20161026
PL  - Australia
TA  - Int J Biol Sci
JT  - International journal of biological sciences
JID - 101235568
RN  - 0 (Iridoid Glucosides)
RN  - 0 (Reactive Oxygen Species)
RN  - 2415-24-9 (catalpol)
RN  - 4Y8F71G49Q (Malondialdehyde)
RN  - EC 1.13.11.31 (Arachidonate 12-Lipoxygenase)
RN  - IY9XDZ35W2 (Glucose)
RN  - S88TT14065 (Oxygen)
SB  - IM
MH  - Animals
MH  - Arachidonate 12-Lipoxygenase/metabolism
MH  - Blotting, Western
MH  - Flow Cytometry
MH  - Glucose/metabolism
MH  - Immunohistochemistry
MH  - In Situ Nick-End Labeling
MH  - Iridoid Glucosides/*pharmacology
MH  - MAP Kinase Signaling System/drug effects
MH  - Malondialdehyde/metabolism
MH  - Membrane Potential, Mitochondrial/drug effects
MH  - Microscopy, Electron, Transmission
MH  - Oligodendroglia/cytology/*drug effects/*metabolism
MH  - Oxidative Stress/drug effects
MH  - Oxygen/metabolism
MH  - Rats
MH  - Reactive Oxygen Species/metabolism
MH  - Signal Transduction/drug effects
MH  - Stem Cells/drug effects/metabolism
PMC - PMC5166484
OTO - NOTNLM
OT  - ERK1/2
OT  - catalpol
OT  - oxidative stress
OT  - oxygen-glucose deprivation
OT  - pre-myelinating oligodendrocytes
COIS- The authors have declared that no competing interest exists.
EDAT- 2016/12/21 06:00
MHDA- 2017/10/21 06:00
PMCR- 2016/01/01
CRDT- 2016/12/21 06:00
PHST- 2016/07/12 00:00 [received]
PHST- 2016/09/06 00:00 [accepted]
PHST- 2016/12/21 06:00 [entrez]
PHST- 2016/12/21 06:00 [pubmed]
PHST- 2017/10/21 06:00 [medline]
PHST- 2016/01/01 00:00 [pmc-release]
AID - ijbsv12p1415 [pii]
AID - 10.7150/ijbs.16823 [doi]
PST - epublish
SO  - Int J Biol Sci. 2016 Oct 26;12(12):1415-1426. doi: 10.7150/ijbs.16823. 
      eCollection 2016.