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.

Regulation of progranulin expression and location by sortilin in oxygen–glucose deprivation/reoxygenation injury

2020 ◽  
Vol 738 ◽  
pp. 135394
Author(s):  
Yan Wang ◽  
Xiaoqing Wang ◽  
Yingbo Li ◽  
Di Chen ◽  
Zhao Liu ◽  
...  
Keyword(s):  
Glucose Deprivation ◽  
Oxygen Glucose Deprivation ◽  
Reoxygenation Injury

scholarly journals Upregulation of miR-216a exerts neuroprotective effects against ischemic injury through negatively regulating JAK2/STAT3-involved apoptosis and inflammatory pathways

2019 ◽  
Vol 130 (3) ◽  
pp. 977-988 ◽  
Author(s):  
Yu Shuang Tian ◽  
Di Zhong ◽  
Qing Qing Liu ◽  
Xiu Li Zhao ◽  
Hong Xue Sun ◽  
...  
Keyword(s):  
Ischemic Stroke ◽  
Inflammatory Mediators ◽  
Neurological Deficit ◽  
Ischemic Injury ◽  
Glucose Deprivation ◽  
Luciferase Assay ◽  
Oxygen Glucose Deprivation ◽  
Tnf Α

OBJECTIVEIschemic stroke remains a significant cause of death and disability in industrialized nations. Janus tyrosine kinase (JAK) and signal transducer and activator of transcription (STAT) of the JAK2/STAT3 pathway play important roles in the downstream signal pathway regulation of ischemic stroke–related inflammatory neuronal damage. Recently, microRNAs (miRNAs) have emerged as major regulators in cerebral ischemic injury; therefore, the authors aimed to investigate the underlying molecular mechanism between miRNAs and ischemic stroke, which may provide potential therapeutic targets for ischemic stroke.METHODSThe JAK2- and JAK3-related miRNA (miR-135, miR-216a, and miR-433) expression levels were detected by real-time quantitative reverse-transcriptase polymerase chain reaction (qRT-PCR) and Western blot analysis in both oxygen-glucose deprivation (OGD)–treated primary cultured neuronal cells and mouse brain with middle cerebral artery occlusion (MCAO)–induced ischemic stroke. The miR-135, miR-216a, and miR-433 were determined by bioinformatics analysis that may target JAK2, and miR-216a was further confirmed by 3′ untranslated region (3′UTR) dual-luciferase assay. The study further detected cell apoptosis, the level of lactate dehydrogenase, and inflammatory mediators (inducible nitric oxide synthase [iNOS], matrix metalloproteinase–9 [MMP-9], tumor necrosis factor–α [TNF-α], and interleukin-1β [IL-1β]) after cells were transfected with miR-NC (miRNA negative control) or miR-216a mimics and subjected to oxygen-glucose deprivation/reoxygenation (OGD/R) damage with 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay, annexin V–FITC/PI, Western blots, and enzyme-linked immunosorbent assay detection. Furthermore, neurological deficit detection and neurological behavior grading were performed to determine the infarction area and neurological deficits.RESULTSJAK2 showed its highest level while miR-216a showed its lowest level at day 1 after ischemic reperfusion. However, miR-135 and miR-433 had no obvious change during the process. The luciferase assay data further confirmed that miR-216a can directly target the 3′UTR of JAK2, and overexpression of miR-216a repressed JAK2 protein levels in OGD/R-treated neuronal cells as well as in the MCAO model ischemic region. In addition, overexpression of miR-216a mitigated cell apoptosis both in vitro and in vivo, which was consistent with the effect of knockdown of JAK2. Furthermore, the study found that miR-216a obviously inhibited the inflammatory mediators after OGD/R, including inflammatory enzymes (iNOS and MMP-9) and cytokines (TNF-α and IL-1β). Upregulating miR-216a levels reduced ischemic infarction and improved neurological deficit.CONCLUSIONSThese findings suggest that upregulation of miR-216a, which targets JAK2, could induce neuroprotection against ischemic injury in vitro and in vivo, which provides a potential therapeutic target for ischemic stroke.

Piezo1 mediates neuron oxygen-glucose deprivation/reoxygenation injury via Ca2+/calpain signaling

2019 ◽  
Vol 513 (1) ◽  
pp. 147-153 ◽  
Author(s):  
Ying-Ying Wang ◽  
Hao Zhang ◽  
Tao Ma ◽  
Yan Lu ◽  
Hou-Yun Xie ◽  
...  
Keyword(s):  
Glucose Deprivation ◽  
Oxygen Glucose Deprivation ◽  
Reoxygenation Injury

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 Silencing of Long Noncoding RNA Nespas Aggravates Microglial Cell Death and Neuroinflammation in Ischemic Stroke

Stroke ◽  
2019 ◽  
Vol 50 (7) ◽  
pp. 1850-1858 ◽  
Author(s):  
Yiming Deng ◽  
Duanduan Chen ◽  
Luyao Wang ◽  
Feng Gao ◽  
Bo Jin ◽  
...  
Keyword(s):  
Cell Death ◽  
Ischemic Stroke ◽  
Middle Cerebral Artery ◽  
Long Noncoding Rna ◽  
Noncoding Rna ◽  
Noncoding Rnas ◽  
Glucose Deprivation ◽  
Artery Occlusion ◽  
Oxygen Glucose Deprivation ◽  
Cerebral Artery Occlusion

Background and Purpose— Ischemic stroke is one of the leading causes of morbidity and mortality worldwide and a major cause of long-term disability. Recently, long noncoding RNAs have been revealed, which are tightly associated with several human diseases. However, the functions of long noncoding RNAs in ischemic stroke still remain largely unknown. In the current study, for the first time, we investigated the role of long noncoding RNA Nespas in ischemic stroke. Methods— We used in vivo models of middle cerebral artery occlusion and in vitro models of oxygen-glucose deprivation to illustrate the effect of long noncoding RNA Nespas on ischemic stroke. Results— We found expression of Nespas was significantly increased in ischemic cerebral tissues and oxygen-glucose deprivation–treated BV2 cells in a time-dependent manner. Silencing of Nespas aggravated middle cerebral artery occlusion operation–induced IR injury and cell death. In addition, proinflammatory cytokine production and NF-κB (nuclear factor-κB) signaling activation were inhibited by Nespas overexpression. TAK1 (transforming growth factor-β–activated kinase 1) was found to directly interact with Nespas, and TAK1 activation was significantly suppressed by Nespas. At last, we found Nespas-inhibited TRIM8 (tripartite motif 8)-induced K63-linked polyubiquitination of TAK1. Conclusions— We showed that Nespas played anti-inflammatory and antiapoptotic roles in cultured microglial cells after oxygen-glucose deprivation stimulation and in mice after ischemic stroke by inhibiting TRIM8-related K63-linked polyubiquitination of TAK1.

scholarly journals Expression and Distribution Pattern of Pnn in Ischemic Cerebral Cortex and Cultured Neural Cells Exposed to Oxygen-Glucose Deprivation

2020 ◽  
Vol 10 (10) ◽  
pp. 708
Author(s):  
Shu-Yuan Hsu ◽  
Sujira Mukda ◽  
Steve Leu
Keyword(s):  
Ischemic Stroke ◽  
Mouse Model ◽  
Glucose Deprivation ◽  
Expression Level ◽  
Oxygen Glucose Deprivation ◽  
Neural Cells ◽  
Nuclear Speckle ◽  
Different Types ◽  
Cellular Apoptosis ◽  
Ischemic Stress

Pinin (Pnn), a multifunctional protein, participates in embryonic development as well as in cellular apoptosis, proliferation, and migration through regulating mRNA alternative splicing and gene transcription. Previous studies have shown that Pnn plays important roles in neural system development and the expression level of Pnn in astrocytes is altered by ischemic stress and associated with cellular apoptosis. In the present study, we further utilized primary cultured rat neurons and astrocytes with oxygen-glucose deprivation (OGD) and a mouse model with middle cerebral artery occlusion (MCAO)-induced ischemic stroke to examine the effect of ischemic stress on Pnn expression and distribution in different types of neural cells. Under normoxia, Pnn is mainly localized in the nuclear speckle of primary cultured neurons. The expression level of Pnn was increased after the OGD treatment and then decreased in the reoxygenation period. Moreover, the cytoplasmic expression of Pnn was observed in neurons with OGD and reoxygenation (OGD/R). Unlike that in neurons, the Pnn expression in astrocytes was decreased after OGD treatment and then gradually increased during the reoxygenation period. Of interest, the nuclear–cytoplasmic translocation of Pnn was not observed in astrocytes with OGD/R. In the MCAO mouse model, the neuronal expression of Pnn in the peri-ischemic region was reduced by three days post induction of ischemic stroke. However, the Pnn expression in astrocytes was not altered. Moreover, the nuclear speckle distribution of Pnn in neurons was also diminished following ischemic stroke. In conclusion, the Pnn expression and distribution after OGD and during reoxygenation showed distinct manners in neurons and astrocytes, implying that Pnn may play different roles in different types of neural cells in the stress response to ischemic injury.

scholarly journals Effects of estradiol on ischemic factor-induced astrocyte swelling and AQP4 protein abundance

2011 ◽  
Vol 301 (1) ◽  
pp. C204-C212 ◽  
Author(s):  
Jennifer M. Rutkowsky ◽  
Breanna K. Wallace ◽  
Phyllis M. Wise ◽  
Martha E. O'Donnell
Keyword(s):  
Ischemic Stroke ◽  
Cell Volume ◽  
Cerebral Edema ◽  
Glucose Deprivation ◽  
Aquaporin 4 ◽  
Oxygen Glucose Deprivation ◽  
Protein Abundance ◽  
Astrocyte Swelling ◽  
Aqp4 Protein ◽  
Stimulation Of

In the early hours of ischemic stroke, cerebral edema forms as Na, Cl, and water are secreted across the blood-brain barrier (BBB) and astrocytes swell. We have shown previously that ischemic factors, including hypoxia, aglycemia, and arginine vasopressin (AVP), stimulate BBB Na-K-Cl cotransporter (NKCC) and Na/H exchanger (NHE) activities and that inhibiting NKCC and/or NHE by intravenous bumetanide and/or HOE-642 reduces edema and infarct in a rat model of ischemic stroke. Estradiol also reduces edema and infarct in this model and abolishes ischemic factor stimulation of BBB NKCC and NHE. There is evidence that NKCC and NHE also participate in ischemia-induced swelling of astrocytes. However, little is known about estradiol effects on astrocyte cell volume. In this study, we evaluated the effects of AVP (100 nM), hypoxia (7.5% O2), aglycemia, hypoxia (2%)/aglycemia [oxygen glucose deprivation (OGD)], and estradiol (1–100 nM) on astrocyte cell volume using 3- O-methyl-d-[3H]glucose equilibration methods. We found that AVP, hypoxia, aglycemia, and OGD (30 min to 5 h) each significantly increased astrocyte cell volume, and that estradiol (30–180 min) abolished swelling induced by AVP or hypoxia, but not by aglycemia or OGD. Bumetanide and/or HOE-642 also abolished swelling induced by AVP but not aglycemia. Abundance of aquaporin-4, known to participate in ischemia-induced astrocyte swelling, was significantly reduced following 7-day but not 2- or 3-h estradiol exposures. Our findings suggest that hypoxia, aglycemia, and AVP each contribute to ischemia-induced astrocyte swelling, and that the edema-attenuating effects of estradiol include reduction of hypoxia- and AVP-induced astrocyte swelling and also reduction of aquaporin-4 abundance.

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