scholarly journals Pretreated fucoidan confers neuroprotection against transient global cerebral ischemic injury in the gerbil hippocampal CA1 area via reducing of glial cell activation and oxidative stress

2019 ◽  
Vol 109 ◽  
pp. 1718-1727 ◽  
Author(s):  
Hyunjung Kim ◽  
Ji Hyeon Ahn ◽  
Minah Song ◽  
Dae Won Kim ◽  
Tae-Kyeong Lee ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Glial Cell ◽  
Cell Activation ◽  
Ischemic Injury ◽  
Glial Cell Activation ◽  
Hippocampal Ca1 ◽  
Hippocampal Ca1 Area ◽  
Ca1 Area ◽  
Cerebral Ischemic ◽  
And Oxidative Stress

scholarly journals Glial Cell Activation and Oxidative Stress in Retinal Degeneration Induced by β-Alanine Caused Taurine Depletion and Light Exposure

2021 ◽  
Vol 23 (1) ◽  
pp. 346
Author(s):  
Ana Martínez-Vacas ◽  
Johnny Di Pierdomenico ◽  
Francisco J. Valiente-Soriano ◽  
Manuel Vidal-Sanz ◽  
Serge Picaud ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Glial Cell ◽  
Cell Activation ◽  
Light Exposure ◽  
Retinal Pigment ◽  
Retinal Pigment Epithelial Cells ◽  
Photoreceptor Outer Segments ◽  
Outer Segments ◽  
Glial Cell Activation ◽  
And Oxidative Stress

We investigate glial cell activation and oxidative stress induced by taurine deficiency secondary to β-alanine administration and light exposure. Two months old Sprague-Dawley rats were divided into a control group and three experimental groups that were treated with 3% β-alanine in drinking water (taurine depleted) for two months, light exposed or both. Retinal and external thickness were measured in vivo at baseline and pre-processing with Spectral-Domain Optical Coherence Tomography (SD-OCT). Retinal cryostat cross sections were immunodetected with antibodies against various antigens to investigate microglial and macroglial cell reaction, photoreceptor outer segments, synaptic connections and oxidative stress. Taurine depletion caused a decrease in retinal thickness, shortening of photoreceptor outer segments, microglial cell activation, oxidative stress in the outer and inner nuclear layers and the ganglion cell layer and synaptic loss. These events were also observed in light exposed animals, which in addition showed photoreceptor death and macroglial cell reactivity. Light exposure under taurine depletion further increased glial cell reaction and oxidative stress. Finally, the retinal pigment epithelial cells were Fluorogold labeled and whole mounted, and we document that taurine depletion impairs their phagocytic capacity. We conclude that taurine depletion causes cell damage to various retinal layers including retinal pigment epithelial cells, photoreceptors and retinal ganglion cells, and increases the susceptibility of the photoreceptor outer segments to light damage. Thus, beta-alanine supplements should be used with caution.

Medical Image Analysis of Telmisartan-Induced Protection in Hippocampal CA1 After Chronic Intermittent Hypoxia

2020 ◽  
Vol 10 (12) ◽  
pp. 2849-2854
Author(s):  
Yixiang Zhang ◽  
Yupeng Zhang ◽  
Yiming Zeng ◽  
Xiaoyang Chen ◽  
Wanyu Wang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Spatial Learning ◽  
Intermittent Hypoxia ◽  
Medical Image ◽  
Medical Image Analysis ◽  
Chronic Intermittent Hypoxia ◽  
Control Group ◽  
Hippocampal Ca1 ◽  
Hippocampal Ca1 Area ◽  
Ca1 Area

Objective: In this paper, we evaluate medical image analysis in hippocampus, immunohistochemistry analyzed and oxidative stress-mediated injury induced by chronic intermittent hypoxia on the mouse hippocampal CA1 area and the protective effects of telmisartan (TEL) on oxidative stress-mediated injury. Methodology: C57B6J mice have been randomly categorized as chronic intermittent hypoxia (CIH) group, CIH + telmisartan (CIH + TEL) group, the room air control group and blank control group, and examined during a period of 12 weeks. Brain images were obtained by Computed tomography scan, spatial learning and memory abilities were tested, and p47 NADPH oxidase subunit (p47PHOX) and 8-hydroxy-guanosine (8-OHG) were measured in the hippocampal CA1 area by immunohistochemistry and analyzed by Image-Pro Plus 6.0. Results: (1) After 12 weeks, there were no abnormalities in mice brain by CT scan. (2) Spatial learning ability measured by escape latency from the Morris water maze in the hypoxia group decreased, while intervention with telmisartan improved the hypoxiainduced spatial learning deficit (F = 3.04, P = 0.045). There exist no differences in spatial memory among any groups. (3) p47PHOX immunostaining significantly increased in hippocampal CA1 area after CIH, which was reduced by TEL intervention. (4) CIH significantly increased 8-OHG immunostaining in the hippocampal CA1 area, while intervention with TEL significantly reduced 8-OHG immunostaining. Conclusions: Telmisartan significantly reduced expression of NADPH oxidase p47PHOX and 8-OHG in CIH mice, and improved hippocampusdependent learning, suggesting that telmisartan can reduce CIH-induced neuronal oxidative stress-mediated injury.

scholarly journals Inflammation, oxidative stress, and glial cell activation characterize stellate ganglia from humans with electrical storm

JCI Insight ◽  
2017 ◽  
Vol 2 (18) ◽  
Author(s):  
Olujimi A. Ajijola ◽  
Donald B. Hoover ◽  
Thomas M. Simerly ◽  
T. Christopher Brown ◽  
Jane Yanagawa ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Glial Cell ◽  
Cell Activation ◽  
Electrical Storm ◽  
Stellate Ganglia ◽  
Glial Cell Activation

LncRNA SNHG12 Improves Cerebral Ischemic-reperfusion Injury by Activating SIRT1/FOXO3a Pathway through I nhibition of Autophagy and Oxidative Stress

2020 ◽  
Vol 17 (4) ◽  
pp. 394-401
Author(s):  
Yuanhua Wu ◽  
Yuan Huang ◽  
Jing Cai ◽  
Donglan Zhang ◽  
Shixi Liu ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Molecular Mechanisms ◽  
Ischemia Reperfusion ◽  
Critical Role ◽  
Cell Activity ◽  
Ht22 Cells ◽  
Cerebral Ischemic ◽  
Cerebral Ischemic Reperfusion ◽  
And Oxidative Stress

Background: Ischemia/reperfusion (I/R) injury involves complex biological processes and molecular mechanisms such as autophagy. Oxidative stress plays a critical role in the pathogenesis of I/R injury. LncRNAs are the regulatory factor of cerebral I/R injury. Methods: This study constructs cerebral I/R model to investigate role of autophagy and oxidative stress in cerebral I/R injury and the underline regulatory mechanism of SIRT1/ FOXO3a pathway. In this study, lncRNA SNHG12 and FOXO3a expression was up-regulated and SIRT1 expression was down-regulated in HT22 cells of I/R model. Results: Overexpression of lncRNA SNHG12 significantly increased the cell viability and inhibited cerebral ischemicreperfusion injury induced by I/Rthrough inhibition of autophagy. In addition, the transfected p-SIRT1 significantly suppressed the release of LDH and SOD compared with cells co-transfected with SIRT1 and FOXO3a group and cells induced by I/R and transfected with p-SNHG12 group and overexpression of cells co-transfected with SIRT1 and FOXO3 further decreased the I/R induced release of ROS and MDA. Conclusion: In conclusion, lncRNA SNHG12 increased cell activity and inhibited oxidative stress through inhibition of SIRT1/FOXO3a signaling-mediated autophagy in HT22 cells of I/R model. This study might provide new potential therapeutic targets for further investigating the mechanisms in cerebral I/R injury and provide.

Toll-like receptor 2 contributes to glial cell activation and heme oxygenase-1 expression in traumatic brain injury

2008 ◽  
Vol 431 (2) ◽  
pp. 123-128 ◽  
Author(s):  
Chanhee Park ◽  
Ik-Hyun Cho ◽  
Donghoon Kim ◽  
Eun-Kyeong Jo ◽  
Se-Young Choi ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Glial Cell ◽  
Heme Oxygenase ◽  
Cell Activation ◽  
Heme Oxygenase 1 ◽  
Toll Like Receptor ◽  
Glial Cell Activation ◽  
Toll Like Receptor 2

scholarly journals Oxytocin protects neurons from hypoxic-ischemic brain injury by enhancing inhibitory neurotransmission in neonatal rats

2021 ◽  
Vol 20 (9) ◽  
pp. 1909-1914
Author(s):  
Linhua Xiang ◽  
Rong Wu ◽  
Kangling Liu ◽  
Jing Wang
Keyword(s):  
Protective Effect ◽  
Hippocampal Slices ◽  
Time Lapse ◽  
Oxytocin Receptor ◽  
Neonatal Rats ◽  
Model Group ◽  
Ischemic Brain ◽  
Hippocampal Ca1 ◽  
Hippocampal Ca1 Area ◽  
Ca1 Area

Purpose: To study the protective effect of oxytocin on hypoxic-ischemic brain neuron injury in neonatal rats, and the mechanism of action involved.Methods: Hippocampal slices from neonatal SD rats were cultured in oxygen/glucose-deprived (OGD) solution, leading to establishment of hypoxic-ischemic model of hippocampal slices in vitro. The slices were assigned to 3 groups: control (ACSF solution), model (OGD solution), and oxytocin (OGD solution + 1 μM oxytocin). The effect of oxytocin on vertebral neurons in hippocampal CA1 region of HIBD rats was determined using TOPRO-3 staining, while the effects of oxytocin on hypoxic depolarization (AD) and inhibitory postsynaptic currents (iPSCs) were measured by cell patch clamp technique.Results: The fluorescence intensity of vertebral lamina in hippocampal CA1 area of model group was significantly higher than that of control group, while the corresponding value for oxytocin group was significantly lower than that of model group (p < 0.05). The time lapse before occurrence of AD in hippocampal CA1 area was significantly longer in oxytocin group than in model group, while the time lapse before neuronal AD in oxytocin receptor antagonist group was lower than that in oxytocin group. The frequency and amplitude of iPSCs in oxytocin group were markedly higher than the corresponding control values.Conclusion: Oxytocin exerts protective effect against hypoxic-ischemic brain neuronal damage in neonatal rats by regulating the activation of oxytocin receptor and GABA receptor, and inhibiting nerve transmission. These findings may be of benefit in the development of a suitable therapy for HIBD.

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