Inflammation and Oxidative Stress: Potential Targets for Improving Prognosis After Subarachnoid Hemorrhage

Subarachnoid hemorrhage (SAH) has a high mortality rate and causes long-term disability in many patients, often associated with cognitive impairment. However, the pathogenesis of delayed brain dysfunction after SAH is not fully understood. A growing body of evidence suggests that neuroinflammation and oxidative stress play a negative role in neurofunctional deficits. Red blood cells and hemoglobin, immune cells, proinflammatory cytokines, and peroxidases are directly or indirectly involved in the regulation of neuroinflammation and oxidative stress in the central nervous system after SAH. This review explores the role of various cellular and acellular components in secondary inflammation and oxidative stress after SAH, and aims to provide new ideas for clinical treatment to improve the prognosis of SAH.

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Long term effects of fetal undernutrition on rat heart. Role of hypertension and oxidative stress

PLoS ONE ◽

10.1371/journal.pone.0171544 ◽

2017 ◽

Vol 12 (2) ◽

pp. e0171544 ◽

Cited By ~ 19

Author(s):

Pilar Rodríguez-Rodríguez ◽

Angel L. López de Pablo ◽

Concha F. García-Prieto ◽

Beatriz Somoza ◽

Begoña Quintana-Villamandos ◽

...

Keyword(s):

Oxidative Stress ◽

Rat Heart ◽

Long Term Effects ◽

And Oxidative Stress

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The role of vanin-1 and oxidative stress–related pathways in distinguishing acute and chronic pediatric ITP

Blood ◽

10.1182/blood-2010-09-304931 ◽

2011 ◽

Vol 117 (17) ◽

pp. 4569-4579 ◽

Cited By ~ 60

Author(s):

Bing Zhang ◽

Clara Lo ◽

Lei Shen ◽

Ruchira Sood ◽

Carol Jones ◽

...

Keyword(s):

Oxidative Stress ◽

Gene Expression ◽

Gene Expression Analysis ◽

Mononuclear Cells ◽

Stress Sensor ◽

Chronic Itp ◽

Acute Itp ◽

And Oxidative Stress

Abstract Pediatric immune thrombocytopenia (ITP) is usually self-limited. However, approximately 20% of children develop chronic ITP, which can be associated with significant morbidity because of long-term immunosuppression and splenectomy in refractory cases. To explore the molecular mechanism of chronic ITP compared with acute ITP, we studied 63 pediatric patients with ITP. Gene expression analysis of whole blood revealed distinct signatures for acute and chronic ITP. Oxidative stress–related pathways were among the most significant chronic ITP-associated pathways. Overexpression of VNN1, an oxidative stress sensor in epithelial cells, was most strongly associated with progression to chronic ITP. Studies of normal persons demonstrated VNN1 expression in a variety of blood cells. Exposure of blood mononuclear cells to oxidative stress inducers elicited dramatic up-regulation of VNN1 and down-regulation of PPARγ, indicating a role for VNN1 as a peripheral blood oxidative stress sensor. Assessment of redox state by tandem mass spectrometry demonstrated statistically significant lower glutathione ratios in patients with ITP versus healthy controls; lower glutathione ratios were also seen in untreated patients with ITP compared with recently treated patients. Our work demonstrates distinct patterns of gene expression in acute and chronic ITP and implicates oxidative stress pathways in the pathogenesis of chronic pediatric ITP.

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The role of oxidative stress, inflammation and acetaminophen exposure from birth to early childhood in the induction of autism

Journal of International Medical Research ◽

10.1177/0300060517693423 ◽

2017 ◽

Vol 45 (2) ◽

pp. 407-438 ◽

Cited By ~ 26

Author(s):

William Parker ◽

Chi Dang Hornik ◽

Staci Bilbo ◽

Zoie E. Holzknecht ◽

Lauren Gentry ◽

...

Keyword(s):

Oxidative Stress ◽

Early Childhood ◽

Early Development ◽

Long Term Effects ◽

Small Children ◽

Factors Associated ◽

Wide Range ◽

And Oxidative Stress

The wide range of factors associated with the induction of autism is invariably linked with either inflammation or oxidative stress, and sometimes both. The use of acetaminophen in babies and young children may be much more strongly associated with autism than its use during pregnancy, perhaps because of well-known deficiencies in the metabolic breakdown of pharmaceuticals during early development. Thus, one explanation for the increased prevalence of autism is that increased exposure to acetaminophen, exacerbated by inflammation and oxidative stress, is neurotoxic in babies and small children. This view mandates extreme urgency in probing the long-term effects of acetaminophen use in babies and the possibility that many cases of infantile autism may actually be induced by acetaminophen exposure shortly after birth.

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Neuronal degeneration and oxidative stress in the SNc of 6-OHDA intoxicated rats; improving role of silymarin long-term treatment

Naunyn-Schmiedeberg s Archives of Pharmacology ◽

10.1007/s00210-020-01954-7 ◽

2020 ◽

Vol 393 (12) ◽

pp. 2427-2437 ◽

Cited By ~ 1

Author(s):

Rasool Haddadi ◽

Shahla Eyvari-Brooshghalan ◽

Alireza Mohajjel Nayebi ◽

Mohammadmahdi Sabahi ◽

Sara Ami Ahmadi

Keyword(s):

Oxidative Stress ◽

Neuronal Degeneration ◽

Term Treatment ◽

Long Term Treatment ◽

And Oxidative Stress

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Estrogen Receptor Activation and Tardive Dyskinesia

The Canadian Journal of Psychiatry ◽

10.1177/070674370004500310 ◽

2000 ◽

Vol 45 (3) ◽

pp. 288-290 ◽

Cited By ~ 18

Author(s):

Peter Turrone ◽

Mary V Seeman ◽

Simone Silvestri

Keyword(s):

Oxidative Stress ◽

Tardive Dyskinesia ◽

Estrogen Replacement Therapy ◽

Cell Damage ◽

Receptor Activation ◽

Estrogen Replacement ◽

Potential Influence ◽

The Central Nervous System ◽

And Oxidative Stress

Objective: To undertake a selective review of the epidemiology, etiology, and treatment of tardive dyskinesia (TD), with emphasis on the potential influence of estrogen in its expression. Method: Both Medline and Psycinfo databases were used to search for articles with the following key words: tardive dyskinesia, humans, animals, dopamine, estrogen, estrogen replacement therapy, antioxidants and oxidative stress. Results: The studies reviewed here suggest that estrogen modulates dopamine-mediated behaviours and that it protects against oxidative stress-induced cell damage caused by long-term exposure to antipsychotic medication. Conclusions: Estrogen's multimodal role in the central nervous system may prove useful for the amelioration or prevention of TD. All the evidence suggests that a placebo-controlled, randomized trial with safer forms of estrogen should be conducted in postmenopausal women with TD.

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Neuroinflammation in Sepsis: Molecular Pathways of Microglia Activation

Pharmaceuticals ◽

10.3390/ph14050416 ◽

2021 ◽

Vol 14 (5) ◽

pp. 416

Author(s):

Carolina Araújo Moraes ◽

Camila Zaverucha-do-Valle ◽

Renaud Fleurance ◽

Tarek Sharshar ◽

Fernando Augusto Bozza ◽

...

Keyword(s):

Central Nervous System ◽

Current Knowledge ◽

Brain Dysfunction ◽

Regulatory Mechanisms ◽

Molecular Pathways ◽

Neurological Manifestations ◽

The Central Nervous System ◽

The Brain

Frequently underestimated, encephalopathy or delirium are common neurological manifestations associated with sepsis. Brain dysfunction occurs in up to 80% of cases and is directly associated with increased mortality and long-term neurocognitive consequences. Although the central nervous system (CNS) has been classically viewed as an immune-privileged system, neuroinflammation is emerging as a central mechanism of brain dysfunction in sepsis. Microglial cells are major players in this setting. Here, we aimed to discuss the current knowledge on how the brain is affected by peripheral immune activation in sepsis and the role of microglia in these processes. This review focused on the molecular pathways of microglial activity in sepsis, its regulatory mechanisms, and their interaction with other CNS cells, especially with neuronal cells and circuits.

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Resveratrol restored Nrf2 function, reduced renal inflammation, and mitigated hypertension in spontaneously hypertensive rats

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.00308.2014 ◽

2015 ◽

Vol 308 (10) ◽

pp. R840-R846 ◽

Cited By ~ 41

Author(s):

Apurva A. Javkhedkar ◽

Yasmir Quiroz ◽

Bernardo Rodriguez-Iturbe ◽

Nosratola D. Vaziri ◽

Mustafa F. Lokhandwala ◽

...

Keyword(s):

Oxidative Stress ◽

Spontaneously Hypertensive Rats ◽

Hypertensive Rats ◽

Renal Inflammation ◽

Spontaneously Hypertensive ◽

Term Administration ◽

And Oxidative Stress ◽

Gst Activity

Compelling evidence supports the role of oxidative stress and renal interstitial inflammation in the pathogenesis of hypertension. Resveratrol is a polyphenolic stilbene, which can lower oxidative stress by activating the transcription factor nuclear factor-E2-related factor-2 (Nrf2), the master regulator of numerous genes encoding antioxidant and phase II-detoxifying enzymes and molecules. Given the role of oxidative stress and inflammation in the pathogenesis of hypertension, we conducted this study to test the hypothesis that long-term administration of resveratrol will attenuate renal inflammation and oxidative stress and, hence, progression of hypertension in the young spontaneously hypertensive rats (SHR). SHR and control [Wistar-Kyoto (WKY)] rats were treated for 9 wk with resveratrol or vehicle in their drinking water. Vehicle-treated SHR exhibited renal inflammatory injury and oxidative stress, as evidenced by glomerulosclerosis, tubulointerstitial injury, infiltration of inflammatory cells, and increased levels of renal 8-isoprostane and protein carbonylation. This was associated with reduced antioxidant capacity and downregulations of Nrf2 and phase II antioxidant enzyme glutathione-S-transferase (GST). Resveratrol treatment mitigated renal inflammation and injury, reduced oxidative stress, normalized antioxidant capacity, restored Nrf2 and GST activity, and attenuated the progression of hypertension in SHR. However, resveratrol had no effect on these parameters in WKY rats. In conclusion, development and progression of hypertension in the SHR are associated with inflammation, oxidative stress, and impaired Nrf2-GST activity in the kidney. Long-term administration of resveratrol restores Nrf2 expression, ameliorates inflammation, and attenuates development of hypertension in SHR. Clinical studies are needed to explore efficacy of resveratrol in human hypertension.

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Inhibition of microRNA-155 Alleviates Neurological Dysfunction Following Transient Global Ischemia and Contribution of Neuroinflammation and Oxidative Stress in the Hippocampus

Current Pharmaceutical Design ◽

10.2174/1381612825666190926162229 ◽

2020 ◽

Vol 25 (40) ◽

pp. 4310-4317 ◽

Cited By ~ 4

Author(s):

Lichao Sun ◽

Shouqin Ji ◽

Jihong Xing

Keyword(s):

Oxidative Stress ◽

Brain Edema ◽

Severity Score ◽

Global Ischemia ◽

Signal Pathways ◽

Neurological Severity Score ◽

Tnf Α ◽

Transient Global Ischemia ◽

And Oxidative Stress

Background/Aims: Central pro-inflammatory cytokine (PIC) signal is involved in neurological deficits after transient global ischemia induced by cardiac arrest (CA). The present study was to examine the role of microRNA- 155 (miR-155) in regulating IL-1β, IL-6 and TNF-α in the hippocampus of rats with induction of CA. We further examined the levels of products of oxidative stress 8-isoprostaglandin F2α (8-iso PGF2α, indication of oxidative stress); and 8-hydroxy-2’-deoxyguanosine (8-OHdG, indication of protein oxidation) after cerebral inhibition of miR-155. Methods: CA was induced by asphyxia and followed by cardiopulmonary resuscitation in rats. ELISA and western blot analysis were used to determine the levels of PICs and products of oxidative stress; and the protein expression of NADPH oxidase (NOXs) in the hippocampus. In addition, neurological severity score and brain edema were examined to assess neurological functions. Results: We observed amplification of IL-1β, IL-6 and TNF-α along with 8-iso PGF2α and 8-OHdG in the hippocampus of CA rats. Cerebral administration of miR-155 inhibitor diminished upregulation of PICs in the hippocampus. This also attenuated products of oxidative stress and upregulation of NOX4. Notably, inhibition of miR-155 improved neurological severity score and brain edema and this was linked to signal pathways of PIC and oxidative stress. Conclusion: We showed the significant role of blocking miR-155 signal in improving the neurological function in CA rats likely via inhibition of signal pathways of neuroinflammation and oxidative stress, suggesting that miR-155 may be a target in preventing and/or alleviating development of the impaired neurological functions during CA-evoked global cerebral ischemia.

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

Current Neurovascular Research ◽

10.2174/1567202617666200727142019 ◽

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.

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