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Edaravone Mitigates Hippocampal Neuronal Death and Cognitive Dysfunction by Upregulating BDNF Expression in Neonatal Hypoxic-Ischemic Rats.

Int J Dev Neurosci

February 2025

Department of Digestive and Nutrition, College of Clinical Medicine for Obstetrics & Gynecology and Pediatrics, Fujian Medical University, Fuzhou, Fujian, China.

Neonatal hypoxic-ischemic encephalopathy (HIE) is a severe neurological injury during infancy, often resulting in long-term cognitive deficits. This study aimed to investigate the neuroprotective effects of Edaravone (EDA), a free radical scavenger, and elucidate the potential role of brain-derived neurotrophic factor (BDNF) in mediating these effects in neonatal HIE rats. Using the Rice-Vannucci model, HIE was induced in neonatal rats, followed by immediate administration of EDA after the hypoxic-ischemic insult.

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Unlabelled: Stress affects gastrointestinal (GI) function causing dysmotility, especially in patients. GI motility is regulated by the enteric nervous system (ENS), suggesting that stress alters ENS biology to cause dysmotility. While stress increases glucocorticoid levels through the hypothalamus-pituitary-adrenal axis, how glucocorticoids affect GI motility is not known.

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Background: Perioperative Neurocognitive Disorders (PND) are associated withanesthesia and surgery, especially in the elderly. Astrocyte activation in old mice correlates with PND development. These cells can switch to a pro-inflammatory or an anti-inflammatory phenotype, regulated by the STAT3 pathway.

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The low-affinity neurotrophic receptor CD271 plays a crucial role in the osteogenic differentiation of ectomesenchyme stem cells (EMSCs), which is essential for the development and regeneration of jaw bones. This study aimed to investigate the influence of CD271 on EMSCs osteogenic differentiation and to uncover the underlying mechanisms. CD271-deficient mice exhibited delayed mandibular bone development, with a significantly reduction in the expression of osteogenic makers such as ALP, Col-1, OPN, and RUNX2.

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Brain-derived neurotrophic factor (BDNF) plays an essential role in regulating diverse neuronal functions in an activity-dependent manner. Although BDNF is synthesized primarily in neurons, astrocytes can also supply BDNF through various routes, including the recycling of neuron-derived BDNF. Despite accumulating evidence for astrocytic BDNF uptake and resecretion of neuronal BDNF, the detailed mechanisms underlying astrocytic BDNF recycling remain unclear.

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