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histone/stroke

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Background: Post-stroke cognitive impairment (PSCI) is commonest clinical disorder in which peripheral cholinergic activity is important. Oleuropein (OLP) is polyphenol is present in olive oil. Here we evaluated the effect of OLP in

Therapeutic application of histone deacetylase inhibitors for stroke.

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Histone deacetylases (HDACs) play a key role in the homeostasis of histone acetylation and gene transcription. Histone hypoacetylation and transcriptional dysfunction have been identified in a large number of neurological diseases, including ischemic and hemorrhagic stroke. HDAC inhibitors (HDACi)
Cerebral stroke is a fatal disease with increasing incidence. The study was to investigate the role and mechanism of Histone deacetylase 6 (HDAC6) on experimental stroke-induced brain injury. The recombinant shRNA-HDAC6 or scramble shRNA lentivirus was transfected to ICR mice. Then, the

[Research progress of histone deacetylase 6 inhibitors in the therapy of ischemic stroke].

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The protein acetylation by histone acetyltransferases (HATs) and histone deacetylases (HDACs) plays a significant role in the development and maturation of the nervous system. HDAC6, belonging to class II HDACs, by regulating the survival, differentiation and maturation of neural cells, plays an

The epigenetics of stroke recovery and rehabilitation: from polycomb to histone deacetylases.

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Classical de-afferentation studies, as well as experience-dependent visual plasticity paradigms, have confirmed that both the developing and adult nervous system are capable of unexpected levels of plasticity. This capacity is underscored by the significant spontaneous recovery that can occur in
Post-stroke dementia (PSD) is a common clinical disease and the central cholinergic circuits are important to cognitive function. Icariin (ICA), a flavonoid isolated from Herba Epimedii, was reported to improve cognitive function through modulating the cholinergic system. But there were no studies

Stroke Induces Nuclear Shuttling of Histone Deacetylase 4.

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OBJECTIVE Histone deacetylases (HDACs) 4 and 5 are abundantly expressed in the brain and have been implicated in the regulation of neurodegeneration. Under physiological conditions, HDACs 4 and 5 are expressed in the cytoplasm of brain cells where they cannot directly access chromatin. In response

Class IIa histone deacetylases affect neuronal remodeling and functional outcome after stroke.

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We have previously demonstrated that stroke induces nuclear shuttling of class IIa histone deacetylase 4 (HDAC4). Stroke-induced nuclear shuttling of HDAC4 is positively and significantly correlated with improved indices of neuronal remodeling in the peri-infarct cortex. In this study, using a rat
Ischemic penumbra that surrounds a stroke-induced infarction core is potentially salvageable; however, mechanisms of its formation are not well known. Covalent modifications of histones control chromatin conformation, gene expression and protein synthesis. To study epigenetic processes in ischemic
Stroke is one of the leading reasons of human death. Ischemic penumbra that surrounds the stroke-induced infarction core is potentially salvageable, but molecular mechanisms of its formation are poorly known. Histone acetylation induces chromatin decondensation and stimulates gene expression. We
In ischemic stroke, vascular occlusion rapidly induces tissue infarct. Over the ensuing hours, damage spreads to adjacent tissue and forms transition zone (penumbra), which is potentially salvageable. Epigenetic regulation of chromatin structure controls gene expression and protein synthesis. We

Novel protective effects of histone deacetylase inhibition on stroke and white matter ischemic injury.

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Understanding how epigenetics influences the process and progress of a stroke could yield new targets and therapeutics for use in the clinic. Experimental evidence suggests that inhibitors of zinc-dependent histone deacetylases can protect neurons, axons, and associated glia from the devastating

HDAC2 (Histone deacetylase 2): a critical factor in environmental enrichment-mediated stroke recovery.

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Environmental enrichment (EE) is a generally accepted strategy to promote stroke recovery and its beneficial effect is positively correlated with neuroplasticity. However, the mechanisms underlying it remain elusive. Histone deacetylase 2 (HDAC2), a negative regulator of neuroplasticity, is

Inhibiting Histone Deacetylase 2 (HDAC2) Promotes Functional Recovery From Stroke.

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BACKGROUND Stroke is a leading cause of long-term disability worldwide. However, current therapies that promote functional recovery from stroke are limited to physical rehabilitation. No pharmacological therapy is available. Thus, understanding the role of histone deacetylase 2 (HDAC2) in the
Sodium butyrate (NaB) is a histone deacetylase (HDAC) inhibitor exhibiting anti-inflammatory and neuroprotective effects in a rat ischemic model of stroke as well as a myocardial ischemia model. Although clinical evidence shows that older women are at higher risk for stroke occurrence and greater
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