Catalpol Protects Pre-myelinating Oligodendrocytes against Ischemia-Induced Oxidative Injury through ERK1/2 Signaling Pathway
Open accessAbstract
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.
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Catalpol interferes with mechanisms underlying diabetes, atherosclerosis, and ischemic injury.
“Catalpol, an iridoid glycoside extracted from the roots of Rehmannia glutinosa (Gaertn.) DC. (Plantaginaceae), has been shown to interfere with different mechanisms underlying many pathological conditions such as diabetes, atherosclerosis, and ischemic injury (Cai et al., 2016; Liu et al., 2016; Xue et al., 2016; Yan et al., 2018; Bai et al., 2019; Chen et al., 2020; He et al., 2021).”
From Exploring the Therapeutic Potential of Phytochemicals in Alzheimer’s Disease: Focus on Polyphenols and Monoterpenes (2022) · cites this paper as Cai et al., 2016
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Multifaceted Effects of Catalpol on Promotion of Perforator Flaps Survival in RatsPreprint
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- Authors
- Cai, Q., Ma, T., Li, C., Tian, Y., & Li, H.
- Affiliations
- Army Medical University (CN)
- Corresponding author
- Li, Hongli
- Venue
- International Journal of Biological Sciences
- Publisher
- Ivyspring International Publisher
- Published
- 2016
- Volume
- 12
- Issue
- 12
- Pages
- 1415-1426
- ISSN
- 1449-2288 (ISSN-L)
- PMC
- PMC5166484
- OpenAlex
- W2557227880
- Cited by
- 26
- References
- 52
- Citations by year
- 2026: 1 · 2025: 1 · 2023: 2 · 2022: 3 · 2021: 2 · 2020: 7 · 2019: 5 · 2018: 1 · 2017: 4
- FWCI
- 3.88
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- cc-by-nc
- Locations
- International Journal of Biological Sciences (publishedVersion, cc-by-nc)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Natural Science Foundation of China (31500969, 31271467)
- Chongqing Science and Technology Commission
- Topics
- Health Sciences › Medicine › Pediatrics, Perinatology and Child Health › Neonatal and fetal brain pathology
- Life Sciences › Neuroscience › Neurology › Neurological Disorders and Treatments
- Health Sciences › Medicine › Pathology and Forensic Medicine › Cardiac Ischemia and Reperfusion
- Keywords
- catalpol, cerebral ischemia, oxidative stress, ERK signaling, oxygen-glucose deprivation, ischemia-reperfusion injury, apoptosis, reactive oxygen species, mitochondrial damage, intracellular calcium, PARP1, U0126
- MeSH terms
- Animals, Arachidonate 12-Lipoxygenase, Flow Cytometry, Glucose, Immunohistochemistry, Malondialdehyde, Oligodendroglia, Oxygen, Stem Cells, Blotting, Western, Signal Transduction, Reactive Oxygen Species, Oxidative Stress, In Situ Nick-End Labeling, MAP Kinase Signaling System, Microscopy, Electron, Transmission, Rats, Membrane Potential, Mitochondrial, Iridoid Glucosides
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