Neat1 decreases neuronal apoptosis after oxygen and glucose deprivation

Recent studies have indicated that resveratrol has protective effects against cerebral ischemia/reperfusion injury. However, the best therapeutic time for resveratrol treatment after acute ischemic stroke remains unknown. We aim to investigate whether resveratrol, administrated at different times after neuronal oxygen and glucose deprivation/reoxygenation (OGD/R) reduced neuronal injury in vitro. There were six experimental groups: normal, model, resveratrol pretreatment, resveratrol post-treatment, resveratrol OGD-treatment, and resveratrol whole-processing group. We found that resveratrol in a concentration-dependent manner decreased the activity of lactate dehydrogenase (LDH) and increased the activity of superoxide dismutase (SOD). Moreover, resveratrol, administrated at different times, increased neuronal viability, reduced neuronal apoptosis, upregulated the protein expressions of Nuclear factor erythroid 2-related factor 2 (Nrf-2), NAD(P)H: quinone oxidoreductase 1 (NQO-1), heme oxygenase 1 (HO-1), and Bcl-2, downregulated the protein expression of Caspase-3, and promoted Nrf-2 to transfer into the nuclei from the cytoplasm. The most effective treatment group was the whole-processing treatment group. These results suggest that resveratrol treatment at different times increased neuronal viability and inhibited neuronal apoptosis in vitro, at least in part, via enhancing the activation of the Nrf-2 signaling pathway.

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Blockage of miR-485-5p on Cortical Neuronal Apoptosis Induced by Oxygen and Glucose Deprivation/Reoxygenation Through Inactivating MAPK Pathway

NeuroMolecular Medicine ◽

10.1007/s12017-020-08605-3 ◽

2020 ◽

Author(s):

Jiangliu Yin ◽

Huan Chen ◽

Suonan Li ◽

Shuai Zhang ◽

Xieli Guo

Keyword(s):

Neuronal Apoptosis ◽

Mapk Pathway ◽

Glucose Deprivation ◽

Oxygen And Glucose Deprivation

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Dexmedetomidine Provides Protection to Neurons Against OGD/R-Induced Oxidative Stress and Neuronal Apoptosis

10.21203/rs.3.rs-69398/v1 ◽

2020 ◽

Author(s):

Deming Xu ◽

Changbi Zhou ◽

Juanyun Lin ◽

Wenhui Cai ◽

Wei Lin

Keyword(s):

Oxidative Stress ◽

Neuronal Apoptosis ◽

Survival Rates ◽

Glucose Deprivation ◽

Point Of View ◽

Dependent Manner ◽

Oxygen And Glucose Deprivation ◽

Protein Levels ◽

Related Proteins

Abstract Background: Dexmedetomidine, a potent α2-adrenoceptor (α2-AR) agonist, is extensively used in the operating room (OR) and intensive care unit (ICU) and has applied in several diseases. However, the precise role of dexmedetomidine in oxygen and glucose deprivation/reoxygenation (OGD/R)-treated neurons, and the mechanisms underlying its effect, has yet to be elucidated. Methods: OGD/R-treated neurons served as a cellular model in our study. Western blotting was used to investigate the protein levels of α-adrenergic receptor (α-AR) in OGD/R-treated neurons, apoptosis related proteins (Bcl-2, Bax and Cleaved Caspase 3) and a range of proteins associated with the Nrf2/ARE pathway (Nrf2, HO-1, NQO-1, SOD). The CCK-8 assay was used to determine cell survival rates while Co-IP was used to determine the interactions between α2-AR and Nrf2. The TUNEL assay was used to detect the levels of apoptosis in neurons. Results: OGD/R treatment reduced the level of α2-AR protein in neurons and reduced neuronal survival in a time-dependent manner. However, treatment with dexmedetomidine led to an elevation of α2-AR protein expression in OGD/R-treated neurons and the survival rate of OGD/R-treated neurons. These results indicated that dexmedetomidine treatment promoted the viability of OGD/R-treated neurons but inhibited OGD/R-mediated oxidative stress and neuronal apoptosis. From a mechanistic point-of-view, Nrf2 can bind effectively with α2-AR. We believe that dexmedetomidine exerted effect on the Nrf2/ARE pathway in OGD/R-treated neurons. Silencing the expression of Nrf2 reversed the effects of dexmedetomidine on cell viability, oxidative stress, and neuronal apoptosis in OGD/R-treated neurons.Conclusion: Collectively, our data indicate that elucidated that the activation of α2-AR by dexmedetomidine had a protective effect in neurons against OGD/R-triggered oxidative stress and neuronal apoptosis by modulating the Nrf2/ARE pathway, thus providing a novel way forward to develop clinical therapies to reduce oxidative stress induced by neuronal injury.

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Fyn Kinases Play a Critical Role in Neuronal Apoptosis Induced by Oxygen and Glucose Deprivation or Amyloid-β Peptide Treatment

CNS Neuroscience & Therapeutics ◽

10.1111/j.1755-5949.2012.00357.x ◽

2012 ◽

Vol 18 (9) ◽

pp. 754-761 ◽

Cited By ~ 24

Author(s):

Cai-Ping Du ◽

Ran Tan ◽

Xiao-Yu Hou

Keyword(s):

Neuronal Apoptosis ◽

Critical Role ◽

Amyloid Β ◽

Glucose Deprivation ◽

Amyloid Β Peptide ◽

Oxygen And Glucose Deprivation ◽

Peptide Treatment

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Calycosin-7-O-β-D-glucoside Attenuates OGD/R-Induced Damage by Preventing Oxidative Stress and Neuronal Apoptosis via the SIRT1/FOXO1/PGC-1α Pathway in HT22 Cells

Neural Plasticity ◽

10.1155/2019/8798069 ◽

2019 ◽

Vol 2019 ◽

pp. 1-11

Author(s):

Xiangli Yan ◽

Aiming Yu ◽

Haozhen Zheng ◽

Shengxin Wang ◽

Yingying He ◽

...

Keyword(s):

Oxidative Stress ◽

Neuronal Apoptosis ◽

Ischemia Reperfusion ◽

Glucose Deprivation ◽

Pathological Process ◽

Neuroprotective Effects ◽

Ht22 Cells ◽

Positive Effects ◽

Antioxidant Stress

Neuronal apoptosis induced by oxidative stress is a major pathological process that occurs after cerebral ischemia-reperfusion. Calycosin-7-O-β-D-glucoside (CG) is a representative component of isoflavones in Radix Astragali (RA). Previous studies have shown that CG has potential neuroprotective effects. However, whether CG alleviates neuronal apoptosis through antioxidant stress after ischemia-reperfusion remains unknown. To investigate the positive effects of CG on oxidative stress and apoptosis of neurons, we simulated the ischemia-reperfusion process in vitro using an immortalized hippocampal neuron cell line (HT22) and oxygen-glucose deprivation/reperfusion (OGD/R) model. CG significantly improved cell viability and reduced oxidative stress and neuronal apoptosis. In addition, CG treatment upregulated the expression of SIRT1, FOXO1, PGC-1α, and Bcl-2 and downregulated the expression of Bax. In summary, our findings indicate that CG alleviates OGD/R-induced damage via the SIRT1/FOXO1/PGC-1α signaling pathway. Thus, CG maybe a promising therapeutic candidate for brain injury associated with ischemic stroke.

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