scholarly journals AMPK activation by Tanshinone IIA protects neuronal cells from oxygen-glucose deprivation

Oncotarget ◽  
2017 ◽  
Vol 9 (4) ◽  
pp. 4511-4521 ◽  
Author(s):  
Yingfeng Weng ◽  
Jixian Lin ◽  
Hui Liu ◽  
Hui Wu ◽  
Zhimin Yan ◽  
...  
Keyword(s):  
Neuronal Cells ◽  
Glucose Deprivation ◽  
Tanshinone Iia ◽  
Oxygen Glucose Deprivation ◽  
Ampk Activation

scholarly journals Scoparone protects neuronal cells from oxygen glucose deprivation/reoxygenation injury

RSC Advances ◽  
2019 ◽  
Vol 9 (4) ◽  
pp. 2302-2308 ◽  
Author(s):  
Chunfang Wu ◽  
Ting Li ◽  
Baihui Zhu ◽  
Ruiming Zhu ◽  
Youran Zhang ◽  
...  
Keyword(s):  
Ischemic Stroke ◽  
Causes Of Death ◽  
Neuronal Cells ◽  
Glucose Deprivation ◽  
Oxygen Glucose Deprivation ◽  
The World ◽  
Reoxygenation Injury

Ischemic stroke is one of the leading causes of death and disability in the world.

Higenamine protects neuronal cells from oxygen‐glucose deprivation/reoxygenation‐induced injury

2018 ◽  
Vol 120 (3) ◽  
pp. 3757-3764 ◽  
Author(s):  
Yi Zhang ◽  
Jingjing Zhang ◽  
Chuntao Wu ◽  
Sheng Guo ◽  
Jing Su ◽  
...  
Keyword(s):  
Neuronal Cells ◽  
Glucose Deprivation ◽  
Oxygen Glucose Deprivation

miR-188-5p inhibits apoptosis of neuronal cells during oxygen-glucose deprivation (OGD)-induced stroke by suppressing PTEN

2020 ◽  
Vol 116 ◽  
pp. 104512
Author(s):  
Lijing Li ◽  
Penghua Cui ◽  
Huimin Ge ◽  
Yanjing Shi ◽  
Xiaoguang Wu ◽  
...  
Keyword(s):  
Neuronal Cells ◽  
Glucose Deprivation ◽  
Oxygen Glucose Deprivation

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 Ghrelin Inhibits Apoptosis in Hypothalamic Neuronal Cells during Oxygen-Glucose Deprivation

Endocrinology ◽  
2007 ◽  
Vol 148 (1) ◽  
pp. 148-159 ◽  
Author(s):  
Hyunju Chung ◽  
Eunhee Kim ◽  
Dae Hee Lee ◽  
Sanghee Seo ◽  
Sunghee Ju ◽  
...  
Keyword(s):  
Protein Kinase ◽  
Infarct Volume ◽  
Neuronal Cells ◽  
Reactive Oxygen Species Generation ◽  
Glucose Deprivation ◽  
Positive Energy ◽  
Oxygen Glucose Deprivation ◽  
Cytochrome C Release ◽  
Hypothalamic Neurons ◽  
Antiapoptotic Effect

Ghrelin is an endogenous ligand for the GH secretagogue receptor, produced and secreted mainly from the stomach. Ghrelin stimulates GH release and induces positive energy balances. Previous studies have reported that ghrelin inhibits apoptosis in several cell types, but its antiapoptotic effect in neuronal cells is unknown. Therefore, we investigated the role of ghrelin in ischemic neuronal injury using primary hypothalamic neurons exposed to oxygen-glucose deprivation (OGD). Here we report that treatment of hypothalamic neurons with ghrelin inhibited OGD-induced cell death and apoptosis. Exposure of neurons to ghrelin caused rapid activation of ERK1/2. Ghrelin-induced activation of ERK1/2 and the antiapoptotic effect of ghrelin were blocked by chemical inhibition of MAPK, phosphatidylinositol 3 kinase, protein kinase C, and protein kinase A. Ghrelin attenuated OGD-induced activation of c-Jun NH2-terminal kinase and p-38 but not ERK1/2. We also investigated ghrelin regulation of apoptosis at the mitochondrial level. Ghrelin protected cells from OGD insult by inhibiting reactive oxygen species generation and stabilizing mitochondrial transmembrane potential. In addition, ghrelin-treated cells showed an increased Bcl-2/Bax ratio, prevention of cytochrome c release, and inhibition of caspase-3 activation. Finally, in vivo administration of ghrelin significantly reduced infarct volume in an animal model of ischemia. Our data indicate that ghrelin may act as a survival factor that preserves mitochondrial integrity and inhibits apoptotic pathways.

scholarly journals Targeting cyclophilin-D by compound 19 protects neuronal cells from oxygen glucose deprivation/re-oxygenation

Oncotarget ◽  
2017 ◽  
Vol 8 (52) ◽  
pp. 90238-90249 ◽  
Author(s):  
Jinyu Zheng ◽  
Enhui Cui ◽  
Haikou Yang ◽  
Mao Li ◽  
Jing Zhou ◽  
...  
Keyword(s):  
Neuronal Cells ◽  
Glucose Deprivation ◽  
Oxygen Glucose Deprivation ◽  
Cyclophilin D

scholarly journals Huwe1 interacts with Gadd45b under oxygen-glucose deprivation and reperfusion injury in primary Rat cortical neuronal cells

2015 ◽  
Vol 8 (1) ◽  
Author(s):  
Guo-qian He ◽  
Wen-ming Xu ◽  
Jin-fang Li ◽  
Shuai-shuai Li ◽  
Bin Liu ◽  
...  
Keyword(s):  
Reperfusion Injury ◽  
Neuronal Cells ◽  
Glucose Deprivation ◽  
Oxygen Glucose Deprivation
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