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000271140 1001_ $$0P:(DE-2719)2810557$$aBernis, Maria E.$$b0$$eFirst author$$udzne
000271140 245__ $$aNeuroprotective Effect of Clemastine Improved Oligodendrocyte Proliferation through the MAPK/ERK Pathway in a Neonatal Hypoxia Ischemia Rat Model
000271140 260__ $$aBasel$$bMolecular Diversity Preservation International$$c2024
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000271140 520__ $$aNeonatal 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.
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000271140 650_2 $$2MeSH$$aAnimals
000271140 650_2 $$2MeSH$$aOligodendroglia: drug effects
000271140 650_2 $$2MeSH$$aOligodendroglia: metabolism
000271140 650_2 $$2MeSH$$aNeuroprotective Agents: pharmacology
000271140 650_2 $$2MeSH$$aNeuroprotective Agents: therapeutic use
000271140 650_2 $$2MeSH$$aHypoxia-Ischemia, Brain: drug therapy
000271140 650_2 $$2MeSH$$aHypoxia-Ischemia, Brain: metabolism
000271140 650_2 $$2MeSH$$aHypoxia-Ischemia, Brain: pathology
000271140 650_2 $$2MeSH$$aRats
000271140 650_2 $$2MeSH$$aClemastine: pharmacology
000271140 650_2 $$2MeSH$$aMAP Kinase Signaling System: drug effects
000271140 650_2 $$2MeSH$$aAnimals, Newborn
000271140 650_2 $$2MeSH$$aDisease Models, Animal
000271140 650_2 $$2MeSH$$aCell Proliferation: drug effects
000271140 650_2 $$2MeSH$$aRats, Sprague-Dawley
000271140 7001_ $$0P:(DE-2719)9002687$$aHakvoort, Charlotte$$b1$$udzne
000271140 7001_ $$0P:(DE-2719)9002544$$aNacarkucuk, Efe$$b2$$udzne
000271140 7001_ $$0P:(DE-2719)9002524$$aBurkard, Hannah$$b3$$udzne
000271140 7001_ $$0P:(DE-2719)9001591$$aBremer, Anna-Sophie$$b4$$udzne
000271140 7001_ $$0P:(DE-2719)9000835$$aZweyer, Margit$$b5$$udzne
000271140 7001_ $$0P:(DE-2719)9001055$$aMaes, Elke$$b6$$udzne
000271140 7001_ $$0P:(DE-HGF)0$$aGrzelak, Kora A.$$b7
000271140 7001_ $$0P:(DE-2719)9000732$$aSabir, Hemmen$$b8$$eLast author$$udzne
000271140 770__ $$aMolecular Research and Therapeutic Targets in Acute Settings: Ischemic and Traumatic Brain Injuries
000271140 773__ $$0PERI:(DE-600)2019364-6$$a10.3390/ijms25158204$$gVol. 25, no. 15, p. 8204 -$$n15$$p8204$$tInternational journal of molecular sciences$$v25$$x1422-0067$$y2024
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