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Article

Neuroprotective Effect of Clemastine Improved Oligodendrocyte Proliferation through the MAPK/ERK Pathway in a Neonatal Hypoxia Ischemia Rat Model

1
Neonatologie und Pädiatrische Intensivmedizin, Eltern-Kind-Zentrum, Universitätsklinikum Bonn, 53127 Bonn, Germany
2
Deutsches Zentrum für Neurodegenerative Erkrankungen (DZNE), 53127 Bonn, Germany
*
Author to whom correspondence should be addressed.
These authors contributed equally to this work.
Int. J. Mol. Sci. 2024, 25(15), 8204; https://doi.org/10.3390/ijms25158204 (registering DOI)
Submission received: 8 May 2024 / Revised: 16 July 2024 / Accepted: 20 July 2024 / Published: 27 July 2024

Abstract

Neonatal hypoxic-ischemic encephalopathy is the most common cause of long-term disability in term neonates, and white matter injury is the primary cause of cerebral palsy. Therapies that focus on the neuroprotection of myelination and oligodendrocyte proliferation could potentially ameliorate long-lasting neurological impairments after hypoxic-ischemic encephalopathy. Clemastine, a histamine H1 antagonist, has been shown to exert neuroprotective effects in multiple sclerosis and spinal cord injury by promoting oligodendrogenesis and re-myelination. In this study, we demonstrated the neuroprotective effects of clemastine in our rat model of neonatal hypoxic-ischemic brain injury. Animals received a single intraperitoneal injection of either vehicle or clemastine (10 mg/kg) for 6 consecutive days. Our results showed a significant reduction in white matter loss after treatment, with a clear effect of clemastine on oligodendrocytes, showing a significant increase in the number of Olig2+ cells. We characterized the MAPK/ERK pathway as a potential mechanistic pathway underlying the neuroprotective effects of clemastine. Altogether, our results demonstrate that clemastine is a potential compound for the treatment of hypoxic-ischemic encephalopathy, with a clear neuroprotective effect on white matter injury by promoting oligodendrogenesis.
Keywords: hypoxia; ischemia; white matter; injury; oligodendrogenesis; clemastine; neuroprotective hypoxia; ischemia; white matter; injury; oligodendrogenesis; clemastine; neuroprotective

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MDPI and ACS Style

Bernis, M.E.; Hakvoort, C.; Nacarkucuk, E.; Burkard, H.; Bremer, A.-S.; Zweyer, M.; Maes, E.; Grzelak, K.A.; Sabir, H. Neuroprotective Effect of Clemastine Improved Oligodendrocyte Proliferation through the MAPK/ERK Pathway in a Neonatal Hypoxia Ischemia Rat Model. Int. J. Mol. Sci. 2024, 25, 8204. https://doi.org/10.3390/ijms25158204

AMA Style

Bernis ME, Hakvoort C, Nacarkucuk E, Burkard H, Bremer A-S, Zweyer M, Maes E, Grzelak KA, Sabir H. Neuroprotective Effect of Clemastine Improved Oligodendrocyte Proliferation through the MAPK/ERK Pathway in a Neonatal Hypoxia Ischemia Rat Model. International Journal of Molecular Sciences. 2024; 25(15):8204. https://doi.org/10.3390/ijms25158204

Chicago/Turabian Style

Bernis, Maria E., Charlotte Hakvoort, Efe Nacarkucuk, Hannah Burkard, Anna-Sophie Bremer, Margit Zweyer, Elke Maes, Kora A. Grzelak, and Hemmen Sabir. 2024. "Neuroprotective Effect of Clemastine Improved Oligodendrocyte Proliferation through the MAPK/ERK Pathway in a Neonatal Hypoxia Ischemia Rat Model" International Journal of Molecular Sciences 25, no. 15: 8204. https://doi.org/10.3390/ijms25158204

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