scholarly journals Neuregulin 1/ErbB4 signaling attenuates neuronal cell damage under oxygen-glucose deprivation in primary hippocampal neurons

2019 ◽  
Vol 52 (4) ◽  
pp. 462 ◽  
Author(s):  
Ji-Young Yoo ◽  
Han-Byeol Kim ◽  
Seung-Yeon Yoo ◽  
Hong-Il Yoo ◽  
Dae-Yong Song ◽  
...  
Keyword(s):  
Hippocampal Neurons ◽  
Cell Damage ◽  
Neuronal Cell ◽  
Glucose Deprivation ◽  
Oxygen Glucose Deprivation ◽  
Neuregulin 1 ◽  
Primary Hippocampal Neurons

scholarly journals K6PC-5 Activates SphK1-Nrf2 Signaling to Protect Neuronal Cells from Oxygen Glucose Deprivation/Re-Oxygenation

2018 ◽  
Vol 51 (4) ◽  
pp. 1908-1920 ◽  
Author(s):  
Hua Liu ◽  
Zhiqing Zhang ◽  
Min Xu ◽  
Rong Xu ◽  
Zhichun Wang ◽  
...  
Keyword(s):  
Hippocampal Neurons ◽  
Ischemia Reperfusion ◽  
Neuronal Cells ◽  
Neuronal Cell ◽  
Glucose Deprivation ◽  
Cell Counting ◽  
Oxygen Glucose Deprivation ◽  
Related Factor ◽  
Cell Protection ◽  
Neuroprotective Strategy

Background/Aims: New strategies are required to combat neuronal ischemia-reperfusion injuries. K6PC-5 is a novel sphingosine kinase 1 (SphK1) activator whose potential activity in neuronal cells has not yet been tested. Methods: Cell survival and necrosis were assessed with a Cell Counting Kit-8 assay and lactate dehydrogenase release assay, respectively. Mitochondrial depolarization was tested by a JC-1 dye assay. Expression levels of nuclear factor erythroid 2-related factor 2 (Nrf2) signaling components were examined by quantitative real-timePCR and western blotting. Results: K6PC-5 protected SH-SY5Y neuronal cells and primary murine hippocampal neurons from oxygen glucose deprivation/re-oxygenation (OGDR). K6PC-5 activated SphK1, and SphK1 knockdown by targeted short hairpin RNA (shRNA) almost completely abolished K6PC-5-induced neuronal cell protection. Further work showed that K6PC-5 inhibited OGDR-induced programmed necrosis in neuronal cells. Importantly, K6PC-5 activated Nrf2 signaling, which is downstream of SphK1. Silencing of Nrf2 by targeted shRNA almost completely nullified K6PC-5-mediated neuronal cell protection against OGDR. Conclusion: K6PC-5 activates SphK1-Nrf2 signaling to protect neuronal cells from OGDR. K6PC-5 might be a promising neuroprotective strategy for ischemia-reperfusion injuries.

scholarly journals Synaptic P2X7 and Oxygen/Glucose Deprivation in Organotypic Hippocampal Cultures

2004 ◽  
Vol 24 (4) ◽  
pp. 392-398 ◽  
Author(s):  
Fabio Cavaliere ◽  
Susanna Amadio ◽  
Giuseppe Sancesario ◽  
Giorgio Bernardi ◽  
Cinzia Volonté
Keyword(s):  
Ex Vivo ◽  
Cell Damage ◽  
Neuronal Cell ◽  
Glucose Deprivation ◽  
Cellular Damage ◽  
Confocal Laser ◽  
Oxygen Glucose Deprivation ◽  
Ex Vivo Model ◽  
Reactive Blue 2 ◽  
Hippocampal Cultures

The P2X7 receptor for extracellular ATP is the main candidate, among P2 receptors, inducing cell death in the immune system. Here, we demonstrate the direct participation of this receptor to cell damage induced by oxygen/glucose deprivation, in the ex vivo model of organotypic hippocampal cultures. By pharmacological and immunological approaches, we show that P2X7 is rapidly and transiently up regulated in hippocampal areas eliciting metabolism impairment. Moreover, the P2 antagonists 2′,3′,-dialdehyde ATP and reactive blue 2 prevent both up regulation of this receptor and hypoxic/hypoglycemic damage. By confocal laser microscopy, we show that P2X7 is present at the synaptic level of fibers extending from the CA1–2 pyramidal cell layer throughout the strata oriens and radiatum, but absent on oligodendrocytes, astrocytes or neuronal cell bodies. Colocalization of P2X7 is obtained with neurofilament-L protein and with synaptophysin, not with myelin basic protein, glial fibrillary acidic protein or a marker for neuronal nuclei. P2X7 up regulation and diffuse cellular damage are also induced by 3′-O-(4-benzoyl) benzoyl-ATP, an agonist selective but not exclusive for P2X7. In summary, our study demonstrates that P2X7 not only directly participates to the hypoxic/hypoglycemic process, but also owns specific phenotypic localization. We do not exclude that it might serve as a sensor of dysregulated neuronal activity and ATP release, both occurring during oxygen/glucose deprivation.

Neurotrophic Properties of Silexan, an Essential Oil from the Flowers of Lavender-Preclinical Evidence for Antidepressant-Like Properties

2020 ◽  
Vol 54 (01) ◽  
pp. 37-46
Author(s):  
Kristina Friedland ◽  
Giacomo Silani ◽  
Anita Schuwald ◽  
Carola Stockburger ◽  
Egon Koch ◽  
...  
Keyword(s):  
Essential Oil ◽  
Hippocampal Neurons ◽  
Day Treatment ◽  
Neuronal Cell ◽  
Antidepressant Activity ◽  
In Vivo Models ◽  
Antidepressant Effects ◽  
Primary Hippocampal Neurons

Abstract Background Silexan, a special essential oil from flowering tops of lavandula angustifolia, is used to treat subsyndromal anxiety disorders. In a recent clinical trial, Silexan also showed antidepressant effects in patients suffering from mixed anxiety-depression (ICD-10 F41.2). Since preclinical data explaining antidepressant properties of Silexan are missing, we decided to investigate if Silexan also shows antidepressant-like effects in vitro as well as in vivo models. Methods We used the forced swimming test (FST) in rats as a simple behavioral test indicative of antidepressant activity in vivo. As environmental events and other risk factors contribute to depression through converging molecular and cellular mechanisms that disrupt neuronal function and morphology—resulting in dysfunction of the circuitry that is essential for mood regulation and cognitive function—we investigated the neurotrophic properties of Silexan in neuronal cell lines and primary hippocampal neurons. Results The antidepressant activity of Silexan (30 mg/kg BW) in the FST was comparable to the tricyclic antidepressant imipramine (20 mg/kg BW) after 9-day treatment. Silexan triggered neurite outgrowth and synaptogenesis in 2 different neuronal cell models and led to a significant increase in synaptogenesis in primary hippocampal neurons. Silexan led to a significant phosphorylation of protein kinase A and subsequent CREB phosphorylation. Conclusion Taken together, Silexan demonstrates antidepressant-like effects in cellular as well as animal models for antidepressant activity. Therefore, our data provides preclinical evidence for the clinical antidepressant effects of Silexan in patients with mixed depression and anxiety.

Daphnetin protects hippocampal neurons from oxygen‐glucose deprivation–induced injury

2018 ◽  
Vol 120 (3) ◽  
pp. 4132-4139 ◽  
Author(s):  
Jin Zhi ◽  
Bin Duan ◽  
Jiwen Pei ◽  
Songdi Wu ◽  
Junli Wei
Keyword(s):  
Hippocampal Neurons ◽  
Glucose Deprivation ◽  
Oxygen Glucose Deprivation
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