The Protective Effects of Apremilast Against Oxygen–Glucose Deprivation/Reperfusion (OGD/R)-Induced Inflammation and Apoptosis in Astroglia Mediated by CREB/BDNF

2021 ◽  
Author(s):  
Hang Yin ◽  
Hao Qin ◽  
Tiantian Wang ◽  
Qiang Zhuang ◽  
Qixia Yang
Keyword(s):  
Glucose Deprivation ◽  
Oxygen Glucose Deprivation ◽  
Protective Effects

scholarly journals Kaempferol Ameliorates Oxygen-Glucose Deprivation/Reoxygenation-Induced Neuronal Ferroptosis by Activating Nrf2/SLC7A11/GPX4 Axis

Biomolecules ◽  
2021 ◽  
Vol 11 (7) ◽  
pp. 923
Author(s):  
Yuan Yuan ◽  
Yanyu Zhai ◽  
Jingjiong Chen ◽  
Xiaofeng Xu ◽  
Hongmei Wang
Keyword(s):  
Lipid Peroxidation ◽  
Cell Death ◽  
Antioxidant Capacity ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Nicotinamide Adenine Dinucleotide Phosphate ◽  
Glucose Deprivation ◽  
Oxygen Glucose Deprivation ◽  
Related Factor ◽  
Protective Effects

Kaempferol has been shown to protect cells against cerebral ischemia/reperfusion injury through inhibition of apoptosis. In the present study, we sought to investigate whether ferroptosis is involved in the oxygen-glucose deprivation/reperfusion (OGD/R)-induced neuronal injury and the effects of kaempferol on ferroptosis in OGD/R-treated neurons. Western blot, immunofluorescence, and transmission electron microscopy were used to analyze ferroptosis, whereas cell death was detected using lactate dehydrogenase (LDH) release. We found that OGD/R attenuated SLC7A11 and glutathione peroxidase 4 (GPX4) levels as well as decreased endogenous antioxidants including nicotinamide adenine dinucleotide phosphate (NADPH), glutathione (GSH), and superoxide dismutase (SOD) in neurons. Notably, OGD/R enhanced the accumulation of lipid peroxidation, leading to the induction of ferroptosis in neurons. However, kaempferol activated nuclear factor-E2-related factor 2 (Nrf2)/SLC7A11/GPX4 signaling, augmented antioxidant capacity, and suppressed the accumulation of lipid peroxidation in OGD/R-treated neurons. Furthermore, kaempferol significantly reversed OGD/R-induced ferroptosis. Nevertheless, inhibition of Nrf2 by ML385 blocked the protective effects of kaempferol on antioxidant capacity, lipid peroxidation, and ferroptosis in OGD/R-treated neurons. These results suggest that ferroptosis may be a significant cause of cell death associated with OGD/R. Kaempferol provides protection from OGD/R-induced ferroptosis partly by activating Nrf2/SLC7A11/GPX4 signaling pathway.

scholarly journals The protective effects of GLP-1 receptor agonist lixisenatide on oxygen-glucose deprivation/reperfusion (OGD/R)-induced deregulation of endothelial tube formation

RSC Advances ◽  
2020 ◽  
Vol 10 (17) ◽  
pp. 10245-10253 ◽  
Author(s):  
Mochao Xiao ◽  
Daifeng Lu ◽  
Jiali Tian ◽  
Yang Yu ◽  
Qin Zhang ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Coronary Arteries ◽  
Receptor Agonist ◽  
Glucose Deprivation ◽  
Tube Formation ◽  
Oxygen Glucose Deprivation ◽  
Protective Effects ◽  
Endothelial Tube Formation

Acute myocardial infarction (AMI) is a complication of atherosclerosis that takes place in coronary arteries.

scholarly journals Ginsenosides Rb1 and Rg1 Protect Primary Cultured Astrocytes against Oxygen-Glucose Deprivation/Reoxygenation-Induced Injury via Improving Mitochondrial Function

2019 ◽  
Vol 20 (23) ◽  
pp. 6086 ◽  
Author(s):  
Meng Xu ◽  
Qing Ma ◽  
Chunlan Fan ◽  
Xue Chen ◽  
Huiming Zhang ◽  
...  
Keyword(s):  
Oxidative Phosphorylation ◽  
Cell Viability ◽  
Mitochondrial Function ◽  
Copy Number ◽  
Glucose Deprivation ◽  
Oxygen Glucose Deprivation ◽  
Ros Production ◽  
Protective Effects ◽  
Mtdna Copy Number ◽  
Cultured Astrocytes

This study aimed to evaluate whether ginsenosides Rb1 (20-S-protopanaxadiol aglycon) and Rg1 (20-S-protopanaxatriol aglycon) have mitochondrial protective effects against oxygen-glucose deprivation/reoxygenation (OGD/R)-induced injury in primary mouse astrocytes and to explore the mechanisms involved. The OGD/R model was used to mimic the pathological process of cerebral ischemia-reperfusion in vitro. Astrocytes were treated with normal conditions, OGD/R, OGD/R plus Rb1, or OGD/R plus Rg1. Cell viability was measured to evaluate the cytotoxicity of Rb1 and Rg1. Intracellular reactive oxygen species (ROS) and catalase (CAT) were detected to evaluate oxidative stress. The mitochondrial DNA (mtDNA) copy number and mitochondrial membrane potential (MMP) were measured to evaluate mitochondrial function. The activities of the mitochondrial respiratory chain (MRC) complexes I–V and the level of cellular adenosine triphosphate (ATP) were measured to evaluate oxidative phosphorylation (OXPHOS) levels. Cell viability was significantly decreased in the OGD/R group compared to the control group. Rb1 or Rg1 administration significantly increased cell viability. Moreover, OGD/R caused a significant increase in ROS formation and, subsequently, it decreased the activity of CAT and the mtDNA copy number. At the same time, treatment with OGD/R depolarized the MMP in the astrocytes. Rb1 or Rg1 administration reduced ROS production, increased CAT activity, elevated the mtDNA content, and attenuated the MMP depolarization. In addition, Rb1 or Rg1 administration increased the activities of complexes I, II, III, and V and elevated the level of ATP, compared to those in the OGD/R groups. Rb1 and Rg1 have different chemical structures, but exert similar protective effects against astrocyte damage induced by OGD/R. The mechanism may be related to improved efficiency of mitochondrial oxidative phosphorylation and the reduction in ROS production in cultured astrocytes.

scholarly journals Dexmedetomidine protects against oxygen-glucose deprivation/reoxygenation injury-induced apoptosis via the p38 MAPK/ERK signalling pathway

2017 ◽  
Vol 46 (2) ◽  
pp. 675-686 ◽  
Author(s):  
Ke Wang ◽  
Yuekun Zhu
Keyword(s):  
Cell Survival ◽  
P38 Mapk ◽  
Glucose Deprivation ◽  
Signalling Pathway ◽  
Cell Counting ◽  
Oxygen Glucose Deprivation ◽  
Protective Effects ◽  
N2a Cells ◽  
Induced Apoptosis

Objective To investigate the protective effects of dexmedetomidine (DEX) in oxygen-glucose deprivation/reoxygenation (OGD/R) injury, which is involved in a number of ischaemic diseases. Methods An in vitro OGD/R injury model was generated using mouse Neuro 2A neuroblastoma (N2A) cells. Different concentrations of DEX were administrated to OGD/R cells. CV-65 was used to inhibit p38 microtubule associated protein kinase/extracellular signal-regulated kinases (MAPK/ERK) signalling. Cell proliferation, cell cycle, apoptosis, and the levels of proteins related to p38 MAPK/ERK signalling and apoptosis were evaluated using Cell Counting Kit-8, flow cytometry, TdT-UTP nick end labelling and Western blot analysis, respectively. Results DEX treatment of OGD/R cells promoted cell survival and attenuated OGD/R-induced cell apoptosis. It also activated the p38 MAPK/ERK signalling pathway, increased the levels of Bcl-2, and decreased the levels of Bax and cleaved caspase-3. Treatment with the p38 MAPK/ERK inhibitor CV-65 inhibited the activation of p38 MAPK/ERK and abrogated the DEX-induced effects on cell survival and apoptosis. Conclusions DEX protects N2A cells from OGD/R-induced apoptosis via the activation of the p38 MAPK/ERK signalling pathway. DEX might be an effective agent for the treatment of ischaemic diseases.

s-Methyl cysteine enhanced survival of nerve growth factor differentiated PC12 cells under hypoxic conditions

2014 ◽  
Vol 5 (6) ◽  
pp. 1125-1133 ◽  
Author(s):  
Chun-lin Liu ◽  
Te-chun Hsia ◽  
Mei-chin Yin
Keyword(s):  
Nerve Growth Factor ◽  
Growth Factor ◽  
Cell Line ◽  
Pc12 Cell ◽  
Glucose Deprivation ◽  
Oxygen Glucose Deprivation ◽  
Protective Effects ◽  
Nerve Growth ◽  
Pc12 Cell Line ◽  
Hypoxic Conditions

A nerve growth factor-differentiated PC12 cell line was used to investigate the protective effects ofs-methyl cysteine (SMC) at 1, 2, 4, and 8 μM under oxygen–glucose deprivation (OGD) conditions.

scholarly journals Neuroprotective effects of adenosine deaminase in the striatum

2016 ◽  
Vol 36 (4) ◽  
pp. 709-720 ◽  
Author(s):  
Risa Tamura ◽  
Hiroyuki Ohta ◽  
Yasushi Satoh ◽  
Shigeaki Nonoyama ◽  
Yasuhiro Nishida ◽  
...  
Keyword(s):  
Cerebral Ischemia ◽  
Adenosine Deaminase ◽  
Neuronal Damage ◽  
Brain Slices ◽  
Field Potential ◽  
Glucose Deprivation ◽  
Oxygen Glucose Deprivation ◽  
Protective Effects ◽  
Neuroprotective Effects ◽  
Negative Effect

Adenosine deaminase (ADA) is a ubiquitous enzyme that catabolizes adenosine and deoxyadenosine. During cerebral ischemia, extracellular adenosine levels increase acutely and adenosine deaminase catabolizes the increased levels of adenosine. Since adenosine is a known neuroprotective agent, adenosine deaminase was thought to have a negative effect during ischemia. In this study, however, we demonstrate that adenosine deaminase has substantial neuroprotective effects in the striatum, which is especially vulnerable during cerebral ischemia. We used temporary oxygen/glucose deprivation (OGD) to simulate ischemia in rat corticostriatal brain slices. We used field potentials as the primary measure of neuronal damage. For stable and efficient electrophysiological assessment, we used transgenic rats expressing channelrhodopsin-2, which depolarizes neurons in response to blue light. Time courses of electrically evoked striatal field potential (eFP) and optogenetically evoked striatal field potential (optFP) were recorded during and after oxygen/glucose deprivation. The levels of both eFP and optFP decreased after 10 min of oxygen/glucose deprivation. Bath-application of 10 µg/ml adenosine deaminase during oxygen/glucose deprivation significantly attenuated the oxygen/glucose deprivation-induced reduction in levels of eFP and optFP. The number of injured cells decreased significantly, and western blot analysis indicated a significant decrease of autophagic signaling in the adenosine deaminase-treated oxygen/glucose deprivation slices. These results indicate that adenosine deaminase has protective effects in the striatum.

scholarly journals Mitochondria damaged by Oxygen Glucose Deprivation can be Restored through Activation of the PI3K/Akt Pathway and Inhibition of Calcium Influx by Amlodipine Camsylate

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Hyun-Hee Park ◽  
Myung-Hoon Han ◽  
Hojin Choi ◽  
Young Joo Lee ◽  
Jae Min Kim ◽  
...  
Keyword(s):  
Intracellular Signaling ◽  
Calcium Influx ◽  
Neuroprotective Effect ◽  
Glucose Deprivation ◽  
Structure And Function ◽  
Oxygen Glucose Deprivation ◽  
Protective Effects ◽  
Neuroprotective Effects ◽  
Mitochondrial Structure ◽  
And Function

Abstract Amlodipine, a L-type calcium channel blocker, has been reported to have a neuroprotective effect in brain ischemia. Mitochondrial calcium overload leads to apoptosis of cells in neurologic diseases. We evaluated the neuroprotective effects of amlodipine camsylate (AC) on neural stem cells (NSCs) injured by oxygen glucose deprivation (OGD) with a focus on mitochondrial structure and function. NSCs were isolated from rodent embryonic brains. Effects of AC on cell viability, proliferation, level of free radicals, and expression of intracellular signaling proteins were assessed in OGD-injured NSCs. We also investigated the effect of AC on mitochondrial structure in NSCs under OGD by transmission electron microscopy. AC increased the viability and proliferation of NSCs. This beneficial effect of AC was achieved by strong protection of mitochondria. AC markedly enhanced the expression of mitochondrial biogenesis-related proteins and mitochondrial anti-apoptosis proteins. Together, our results indicate that AC protects OGD-injured NSCs by protecting mitochondrial structure and function. The results of the present study provide insight into the mechanisms underlying the protective effects of AC on NSCs.

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