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valproic acid/hypoxia

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OBJECTIVE Previously, we have documented that prenatal hypoxia can aggravate the cognitive impairment and Alzheimer's disease (AD) neuropathology in APP(Swe) /PS1(A246E) (APP/PS1) transgenic mice, and valproic acid (VPA) can prevent hypoxia-induced down-regulation of β-amyloid (Aβ) degradation
OBJECTIVE Burn-induced gut dysfunction plays an important role in the development of sepsis and multiple organ dysfunction. Emerging evidence suggests that hypoxia-inducible factor-1α (HIF-1α) is critical in paracellular barrier functions via regulating vascular endothelial growth factor (VEGF) and

Suppression of HIF-1α by Valproic Acid Sustains Self-Renewal of Mouse Embryonic Stem Cells under Hypoxia In Vitro.

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The developing embryo naturally experiences relatively low oxygen conditions in vivo. Under in vitro hypoxia, mouse embryonic stem cells (mESCs) lose their self-renewal activity and display an early differentiated morphology mediated by the hypoxia-inducible factor-1α (HIF-1α). Previously, we
OBJECTIVE To evaluate the effects of valproic acid (VPA), a histone deacetylase inhibitor (HDACI), on the expression of hypoxia-inducible factor-1 alpha (HIF-1α) and vascular endothelial growth factor (VEGF) in human retinal Müller cells under hypoxic conditions. METHODS Chemical hypoxia was induced

Valproic acid overcomes hypoxia-induced resistance to apoptosis.

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Valproic acid (VPA), a histone deacetylase inhibitor (HDACi), has been shown to be an effective tool in cancer treatment. Although its ability to induce apoptosis has been described in many cancer types, the data come from experiments performed in normoxic (21% O2) conditions only. Therefore, we
BACKGROUND Pulmonary hypertension (PH) is a serious disease with poor prognosis. Reports show that cells in remodeled pulmonary arteries of PH patients have similar characteristics to cancer cells, such as exuberant inflammation, increased proliferation, and decreased apoptosis. An ideal strategy

Regulation of Neprilysin Activity and Cognitive Functions in Rats After Prenatal Hypoxia.

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The amyloid-degrading enzyme neprilysin (NEP) is one of the therapeutic targets in prevention and treatment of Alzheimer's disease (AD). As we have shown previously NEP expression in rat parietal cortex (Cx) and hippocampus (Hip) decreases with age and is also significantly reduced after prenatal
Gossypol (GOS), a BH3 mimetic, has been investigated as a sensitizing co-therapy to radiation and chemotherapy in treatment of metastatic prostate cancer. In this study, we found that valproic acid (VPA), a histone deacetylase inhibitor (HDACI), counteracted the suppressive effect of GOS on histone

Valproic acid-mediated myocardial protection of acute hemorrhagic rat via the BCL-2 pathway.

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BACKGROUND Hemorrhage is a major cause of morbidity and mortality among trauma patients. The pathophysiologic changes following acute severe hemorrhage and tissue hypoxia lead to an imbalance of protein acetylation. Histone deacetylase inhibitors (HDACIs) were reported to restore the acetylation

Combined Method of Neuronal Cell-Inducible Vector and Valproic Acid for Enhanced Gene Expression under Hypoxic Conditions.

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Gene therapy shows the ability to restore neuronal dysfunction via therapeutic gene expression. The efficiency of gene expression and delivery to hypoxic injury sites is important for successful gene therapy. Therefore, we established a gene/stem cell therapy system using

hif-1 plays a role in hypoxia-induced gustatory plasticity of Caenorhabditis elegans.

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Background: Hypoxia-inducible factor 1 (HIF-1) is a key transcription factor in the detection of low oxygen levels, inducing expression of genes involved in mediating the response to hypoxia to maintain cellular oxygen homeostasis. Caenorhabditis elegans is a soil nematode that has
Antiepileptic drugs (AEDs), such as phenytoin (PHT), carbamazepine (CBZ), trimethadione (TMD), and phenobarbital (PB), have all been associated with a similar pattern of malformations, as well as growth retardation and developmental delay. Valproic acid (VPA) has been associated with a different

Protective effects of valproic acid against hypoxic-ischemic brain injury in neonatal rats.

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Although controversial, protective and therapeutic effects of valproic acid in various types of cellular injury suggest a potential role for this agent in hypoxic-ischemic brain injury. We therefore investigated the effects of valproic acid in an experimental model of neonatal hypoxic-ischemic brain

3',4'-Dimethoxyflavone and valproic acid promotes the proliferation of human hematopoietic stem cells.

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BACKGROUND Human hematopoietic stem cells (HSCs) have been clinically used for transplantation and gene and cellular therapy for more than 4 decades. However, this use is limited because of the challenges in the ex vivo culturing of HSCs. The major hurdle is to amplify these cells without losing

[Protective effects of valproic acid on gut barrier function after major burn injury and its mechanism].

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OBJECTIVE To investigate the potential protective effects of valproic acid (VPA) on gut barrier function after major burn injury in rats and its mechanism. METHODS Forty male Sprague-Dawley (SD) rats were divided into sham + normal saline (NS), sham + VPA, scald + NS, and scald + VPA groups, with 10
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