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International Journal Of Bilogical Sciences

.: Home > International Journal Of Bilogical Sciences > 2016 > Volume 12 Number 12 > Qiyan Cai, Teng Ma, Chengren Li, Yanping Tian, and Hongli Li

Catalpol Protects Pre-Myelinating Oligodendrocytes against Ischemia-induced Oxidative Injury through ERK1/2 Signaling Pathway

Qiyan Cai, Teng Ma, Chengren Li, Yanping Tian, and Hongli Li
Chongqing Key Laboratory of Neurobiology, Department of Histology and Embryology, College of Basic Medicine, The Third Military Medical University, Chongqing, China.  Corresponding author: lihongli@tmmu.edu.cn
Abstract :

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 Ca2+ 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.

Keywords :
catalpol, pre-myelinating oligodendrocytes, oxidative stress, ERK1/2, oxygen-glucose deprivation

Date Deposited : 07 Nov 2016 21:38

Last Modified : 07 Nov 2016 21:38

Official URL: http://www.ijbs.com/v12i12

Volume 12, Number 12, October 2016

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