Journal articles on the topic 'Oxidative Stress Acute brain injuries'
To see the other types of publications on this topic, follow the link: Oxidative Stress Acute brain injuries.
Create a spot-on reference in APA, MLA, Chicago, Harvard, and other styles
Consult the top 50 journal articles for your research on the topic 'Oxidative Stress Acute brain injuries.'
Next to every source in the list of references, there is an 'Add to bibliography' button. Press on it, and we will generate automatically the bibliographic reference to the chosen work in the citation style you need: APA, MLA, Harvard, Chicago, Vancouver, etc.
You can also download the full text of the academic publication as pdf and read online its abstract whenever available in the metadata.
Browse journal articles on a wide variety of disciplines and organise your bibliography correctly.
1
Guo, Hanmu, Lexin Zheng, Heng Xu, Qiuyu Pang, Zhiyang Ren, Yuan Gao, and Tao Wang. "Neurobiological Links between Stress, Brain Injury, and Disease." Oxidative Medicine and Cellular Longevity 2022 (May 25, 2022): 1–17. http://dx.doi.org/10.1155/2022/8111022.
Full textAbstract:
Stress, which refers to a combination of physiological, neuroendocrine, behavioral, and emotional responses to novel or threatening stimuli, is essentially a defensive adaptation under physiological conditions. However, strong and long-lasting stress can lead to psychological and pathological damage. Growing evidence suggests that patients suffering from mild and moderate brain injuries and diseases often show severe neurological dysfunction and experience severe and persistent stressful events or environmental stimuli, whether in the acute, subacute, or recovery stage. Previous studies have shown that stress has a remarkable influence on key brain regions and brain diseases. The mechanisms through which stress affects the brain are diverse, including activation of endoplasmic reticulum stress (ERS), apoptosis, oxidative stress, and excitatory/inhibitory neuron imbalance, and may lead to behavioral and cognitive deficits. The impact of stress on brain diseases is complex and involves impediment of recovery, aggravation of cognitive impairment, and neurodegeneration. This review summarizes various stress models and their applications and then discusses the effects and mechanisms of stress on key brain regions—including the hippocampus, hypothalamus, amygdala, and prefrontal cortex—and in brain injuries and diseases—including Alzheimer’s disease, stroke, traumatic brain injury, and epilepsy. Lastly, this review highlights psychological interventions and potential therapeutic targets for patients with brain injuries and diseases who experience severe and persistent stressful events.
2
Cavalli, Loredana, Lucia Briscese, Tiziana Cavalli, Paolo Andre, and Maria Chiara Carboncini. "Role of Acupuncture in the Management of Severe Acquired Brain Injuries (sABIs)." Evidence-Based Complementary and Alternative Medicine 2018 (September 12, 2018): 1–10. http://dx.doi.org/10.1155/2018/8107508.
Full textAbstract:
Acupuncture therapy has been used to treat several disorders in Asian countries and its use is increasing in Western countries as well. Current literature assessed the safety and efficacy of acupuncture in the acute management and rehabilitation of patients with neurologic disorders. In this paper, the role of acupuncture in the treatment of acute severe acquired brain injuries is described, acting on neuroinflammation, intracranial oedema, oxidative stress, and neuronal regeneration. Moreover, beneficial effects of acupuncture on subacute phase and chronic outcomes have been reported in controlling the imbalance of IGF-1 hormone and in decreasing spasticity, pain, and the incidence of neurovegetative crisis. Moreover, acupuncture may have a positive action on the arousal recovery. Further work is needed to understand the effects of specific acupoints on the brain. Allegedly concurrent neurophysiological measurements (e.g., EEG) may help in studying acupuncture-related changes in central nervous system activity and determining its potential as an add-on rehabilitative treatment for patients with consciousness disorders.
3
Lee, Song-Hee, Min-Woo Lee, Dong-Gyun Ko, Bo-Young Choi, and Sang-Won Suh. "The Role of NADPH Oxidase in Neuronal Death and Neurogenesis after Acute Neurological Disorders." Antioxidants 10, no. 5 (May 7, 2021): 739. http://dx.doi.org/10.3390/antiox10050739.
Full textAbstract:
Oxidative stress is a well-known common pathological process involved in mediating acute neurological injuries, such as stroke, traumatic brain injury, epilepsy, and hypoglycemia-related neuronal injury. However, effective therapeutic measures aimed at scavenging free reactive oxygen species have shown little success in clinical trials. Recent studies have revealed that NADPH oxidase, a membrane-bound enzyme complex that catalyzes the production of a superoxide free radical, is one of the major sources of cellular reactive oxygen species in acute neurological disorders. Furthermore, several studies, including our previous ones, have shown that the inhibition of NADPH oxidase can reduce subsequent neuronal injury in neurological disease. Moreover, maintaining appropriate levels of NADPH oxidase has also been shown to be associated with proper neurogenesis after neuronal injury. This review aims to present a comprehensive overview of the role of NADPH oxidase in neuronal death and neurogenesis in multiple acute neurological disorders and to explore potential pharmacological strategies targeting the NADPH-related oxidative stress pathways.
4
Rjiba-Touati, K., I. Ayed-Boussema, Y. Guedri, A. Achour, H. Bacha, and S. Abid-Essefi. "Effect of recombinant human erythropoietin on mitomycin C-induced oxidative stress and genotoxicity in rat kidney and heart tissues." Human & Experimental Toxicology 35, no. 1 (March 2, 2015): 53–62. http://dx.doi.org/10.1177/0960327115577521.
Full textAbstract:
Mitomycin C (MMC) is an antineoplastic agent used for the treatment of several human malignancies. Nevertheless, the prolonged use of the drug may result in a serious heart and kidney injuries. Recombinant human erythropoietin (rhEPO) has recently been shown to exert an important cytoprotective effect in experimental brain injury and ischemic acute renal failure. The aim of the present work is to investigate the cardioprotective and renoprotective effects of rhEPO against MMC-induced oxidative damage and genotoxicity. Our results showed that MMC induced oxidative stress and DNA damage. rhEPO administration in any treatment conditions decreased oxidative damage induced by MMC. It reduced malondialdehyde and protein carbonyl levels. rhEPO ameliorated reduced glutathione plus oxidized glutathione modulation and the increased catalase activity after MMC treatment. Furthermore, rhEPO restored DNA damage caused by MMC. We concluded that rhEPO administration especially in pretreatment condition protected rats against MMC-induced heart and renal oxidative stress and genotoxicity.
5
Zhang, Kaige, Yiming Jiang, Biyao Wang, Tiange Li, Dehao Shang, and Xinwen Zhang. "Mesenchymal Stem Cell Therapy: A Potential Treatment Targeting Pathological Manifestations of Traumatic Brain Injury." Oxidative Medicine and Cellular Longevity 2022 (June 15, 2022): 1–11. http://dx.doi.org/10.1155/2022/4645021.
Full textAbstract:
Traumatic brain injury (TBI) makes up a large proportion of acute brain injuries and is a major cause of disability globally. Its complicated etiology and pathogenesis mainly include primary injury and secondary injury over time, which can cause cognitive deficits, physical disabilities, mood changes, and impaired verbal communication. Recently, mesenchymal stromal cell- (MSC-) based therapy has shown significant therapeutic potential to target TBI-induced pathological processes, such as oxidative stress, neuroinflammation, apoptosis, and mitochondrial dysfunction. In this review, we discuss the main pathological processes of TBI and summarize the underlying mechanisms of MSC-based TBI treatment. We also discuss research progress in the field of MSC therapy in TBI as well as major shortcomings and the great potential shown.
6
Park, Chang-Hyun, Ji Hoon Song, Su-Nam Kim, Ji Hwan Lee, Hae-Jeung Lee, Ki Sung Kang, and Hyung-Ho Lim. "Neuroprotective Effects of Tetrahydrocurcumin against Glutamate-Induced Oxidative Stress in Hippocampal HT22 Cells." Molecules 25, no. 1 (December 30, 2019): 144. http://dx.doi.org/10.3390/molecules25010144.
Full textAbstract:
In the central nervous system, glutamate is a major excitable neurotransmitter responsible for many cellular functions. However, excessive levels of glutamate induce neuronal cell death via oxidative stress during acute brain injuries as well as chronic neurodegenerative diseases. The present study was conducted to examine the effect of tetrahydrocurcumin (THC), a major secondary metabolite of curcumin, and its possible mechanism against glutamate-induced cell death. We prepared THC using curcumin isolated from Curcuma longa (turmeric) and demonstrated the protective effect of THC against glutamate-induced oxidative stress in HT22 cells. THC abrogated glutamate-induced HT22 cell death and showed a strong antioxidant effect. THC also significantly reduced intracellular calcium ion increased by glutamate. Additionally, THC significantly reduced the accumulation of intracellular oxidative stress induced by glutamate. Furthermore, THC significantly diminished apoptotic cell death indicated by annexin V-positive in HT22 cells. Western blot analysis indicated that the phosphorylation of mitogen-activated protein kinases including c-Jun N-terminal kinase, extracellular signal-related kinases 1/2, and p38 by glutamate was significantly diminished by treatment with THC. In conclusion, THC is a potent neuroprotectant against glutamate-induced neuronal cell death by inhibiting the accumulation of oxidative stress and phosphorylation of mitogen-activated protein kinases.
7
Monsel, Antoine, Ying-gang Zhu, Stephane Gennai, Qi Hao, Jia Liu, and Jae W. Lee. "Cell-based Therapy for Acute Organ Injury." Anesthesiology 121, no. 5 (November 1, 2014): 1099–121. http://dx.doi.org/10.1097/aln.0000000000000446.
Full textAbstract:
Abstract Critically ill patients often suffer from multiple organ failures involving lung, kidney, liver, or brain. Genomic, proteomic, and metabolomic approaches highlight common injury mechanisms leading to acute organ failure. This underlines the need to focus on therapeutic strategies affecting multiple injury pathways. The use of adult stem cells such as mesenchymal stem or stromal cells (MSC) may represent a promising new therapeutic approach as increasing evidence shows that MSC can exert protective effects following injury through the release of promitotic, antiapoptotic, antiinflammatory, and immunomodulatory soluble factors. Furthermore, they can mitigate metabolomic and oxidative stress imbalance. In this work, the authors review the biological capabilities of MSC and the results of clinical trials using MSC as therapy in acute organ injuries. Although preliminary results are encouraging, more studies concerning safety and efficacy of MSC therapy are needed to determine their optimal clinical use. (Anesthesiology 2014; 121:1099-121)
8
Zheng, Yijun, and Duming Zhu. "Molecular Hydrogen Therapy Ameliorates Organ Damage Induced by Sepsis." Oxidative Medicine and Cellular Longevity 2016 (2016): 1–6. http://dx.doi.org/10.1155/2016/5806057.
Full textAbstract:
Since it was proposed in 2007, molecular hydrogen therapy has been widely concerned and researched. Many animal experiments were carried out in a variety of disease fields, such as cerebral infarction, ischemia reperfusion injury, Parkinson syndrome, type 2 diabetes mellitus, metabolic syndrome, chronic kidney disease, radiation injury, chronic hepatitis, rheumatoid arthritis, stress ulcer, acute sports injuries, mitochondrial and inflammatory disease, and acute erythema skin disease and other pathological processes or diseases. Molecular hydrogen therapy is pointed out as there is protective effect for sepsis patients, too. The impact of molecular hydrogen therapy against sepsis is shown from the aspects of basic vital signs, organ functions (brain, lung, liver, kidney, small intestine, etc.), survival rate, and so forth. Molecular hydrogen therapy is able to significantly reduce the release of inflammatory factors and oxidative stress injury. Thereby it can reduce damage of various organ functions from sepsis and improve survival rate. Molecular hydrogen therapy is a prospective method against sepsis.
9
Javaid, Sana, Talha Farooq, Zohabia Rehman, Ammara Afzal, Waseem Ashraf, Muhammad Fawad Rasool, Faleh Alqahtani, et al. "Dynamics of Choline-Containing Phospholipids in Traumatic Brain Injury and Associated Comorbidities." International Journal of Molecular Sciences 22, no. 21 (October 20, 2021): 11313. http://dx.doi.org/10.3390/ijms222111313.
Full textAbstract:
The incidences of traumatic brain injuries (TBIs) are increasing globally because of expanding population and increased dependencies on motorized vehicles and machines. This has resulted in increased socio-economic burden on the healthcare system, as TBIs are often associated with mental and physical morbidities with lifelong dependencies, and have severely limited therapeutic options. There is an emerging need to identify the molecular mechanisms orchestrating these injuries to life-long neurodegenerative disease and a therapeutic strategy to counter them. This review highlights the dynamics and role of choline-containing phospholipids during TBIs and how they can be used to evaluate the severity of injuries and later targeted to mitigate neuro-degradation, based on clinical and preclinical studies. Choline-based phospholipids are involved in maintaining the structural integrity of the neuronal/glial cell membranes and are simultaneously the essential component of various biochemical pathways, such as cholinergic neuronal transmission in the brain. Choline or its metabolite levels increase during acute and chronic phases of TBI because of excitotoxicity, ischemia and oxidative stress; this can serve as useful biomarker to predict the severity and prognosis of TBIs. Moreover, the effect of choline-replenishing agents as a post-TBI management strategy has been reviewed in clinical and preclinical studies. Overall, this review determines the theranostic potential of choline phospholipids and provides new insights in the management of TBI.
10
Rodrigues, Cecilia M. P., Stephen R. Spellman, Susana Solá, Andrew W. Grande, Cheryle Linehan-Stieers, Walter C. Low, and Clifford J. Steer. "Neuroprotection by a Bile Acid in an Acute Stroke Model in the Rat." Journal of Cerebral Blood Flow & Metabolism 22, no. 4 (April 2002): 463–71. http://dx.doi.org/10.1097/00004647-200204000-00010.
Full textAbstract:
Tauroursodeoxycholic acid (TUDCA), a hydrophilic bile acid, is a strong modulator of apoptosis in both hepatic and nonhepatic cells, and appears to function by inhibiting mitochondrial membrane perturbation. Excitotoxicity, metabolic compromise, and oxidative stress are major determinants of cell death after brain ischemia-reperfusion injury. However, some neurons undergo delayed cell death that is characteristic of apoptosis. Therefore, the authors examined whether TUDCA could reduce the injury associated with acute stroke in a well-characterized model of transient focal cerebral ischemia. Their model of middle cerebral artery occlusion resulted in marked cell death with prominent terminal deoxynucleotidyl transferase-mediated 2′-deoxyuridine 5′-triphosphate-biotin nick end labeling (TUNEL) within the ischemic penumbra, mitochondrial swelling, and caspase activation. Tauroursodeoxycholic acid administered 1 hour after ischemia resulted in significantly increased bile acid levels in the brain, improved neurologic function, and an approximately 50% reduction in infarct size 2 and 7 days after reperfusion. In addition, TUDCA significantly reduced the number of TUNEL-positive brain cells, mitochondrial swelling, and partially inhibited caspase-3 processing and substrate cleavage. These findings suggest that the mechanism for in vivo neuroprotection by TUDCA is, in part, mediated by inhibition of mitochondrial perturbation and subsequent caspase activation leading to apoptotic cell death. Thus, TUDCA, a clinically safe molecule, may be useful in the treatment of stroke and possibly other apoptosis-associated acute and chronic injuries to the brain.
11
Yang, Gui-Li, Shizhao Wang, Shu Zhang, Ye Liu, Xiao Liu, Dong Wang, Huijie Wei, et al. "A Protective Role of Tumor Necrosis Factor Superfamily-15 in Intracerebral Hemorrhage-Induced Secondary Brain Injury." ASN Neuro 13 (January 2021): 175909142110384. http://dx.doi.org/10.1177/17590914211038441.
Full textAbstract:
Destabilization of blood vessels by the activities of vascular endothelial growth factor (VEGF) and matrix metalloproteinases (MMPs) following intracerebral hemorrhage (ICH) has been considered the main causes of aggravated secondary brain injury. Here, we show that tumor necrosis factor superfamily-15 (TNFSF15; also known as vascular endothelial growth inhibitor), an inhibitor of VEGF-induced vascular hyper-permeability, when overexpressed in transgenic mice, exhibits a neuroprotective function post-ICH. In this study, we set-up a collagenase-induced ICH model with TNFSF15-transgenic mice and their transgene-negative littermates. We observed less lesion volume and neural function perturbations, together with less severe secondary injuries in the acute phase that are associated with brain edema and inflammation, including vascular permeability, oxidative stress, microglia/macrophage activation and neutrophil infiltration, and neuron degeneration, in the TNFSF15 group compared with the littermate group. Additionally, we show that there is an inhibition of VEGF-induced elevation of MMP-9 in the perihematomal blood vessels of the TNFSF15 mice following ICH, concomitant with enhanced pericyte coverage of the perihematomal blood vessels. These findings are consistent with the view that TNFSF15 may have a potential as a therapeutic agent for the treatment of secondary injuries in the early phase of ICH.
12
Gayen, Manoshi, Manish Bhomia, Nagaraja Balakathiresan, and Barbara Knollmann-Ritschel. "Exosomal MicroRNAs Released by Activated Astrocytes as Potential Neuroinflammatory Biomarkers." International Journal of Molecular Sciences 21, no. 7 (March 27, 2020): 2312. http://dx.doi.org/10.3390/ijms21072312.
Full textAbstract:
Neuroinflammation is a hallmark of several neurodegenerative diseases and disorders, including traumatic brain injury (TBI). Neuroinflammation results in the activation of glial cells which exacerbates the neuroinflammatory process by secretion of pro-inflammatory cytokines and results in disruption of glial transmission networks. The glial cells, including astrocytes, play a critical role in the maintenance of homeostasis in the brain. Activated astrocytes release several factors as part of the inflammatory process including cytokines, proteins, and microRNAs (miRNAs). MiRNAs are noncoding RNA molecules involved in normal physiological processes and disease pathogenesis. MiRNAs have been implicated as important cell signaling molecules, and they are potential diagnostic biomarkers and therapeutic targets for various diseases, including neurological disorders. Exosomal miRNAs released by astrocytic response to neuroinflammation is not yet studied. In this study, primary human astrocytes were activated by IL-1β stimulation and we examined astrocytic exosomal miRNA cargo released in a neuroinflammatory stress model. Results indicate that acute neuroinflammation and oxidative stress induced by IL-1β generates the release of a specific subset of miRNAs via exosomes, which may have a potential role in regulating the inflammatory response. Additionally, these miRNAs may serve as potential biomarkers of neuroinflammation associated with neurological disorders and injuries.
13
Li, Xiaolong, Feifei Yuan, and Lili Zhou. "Organ Crosstalk in Acute Kidney Injury: Evidence and Mechanisms." Journal of Clinical Medicine 11, no. 22 (November 9, 2022): 6637. http://dx.doi.org/10.3390/jcm11226637.
Full textAbstract:
Acute kidney injury (AKI) is becoming a public health problem worldwide. AKI is usually considered a complication of lung, heart, liver, gut, and brain disease, but recent findings have supported that injured kidney can also cause dysfunction of other organs, suggesting organ crosstalk existence in AKI. However, the organ crosstalk in AKI and the underlying mechanisms have not been broadly reviewed or fully investigated. In this review, we summarize recent clinical and laboratory findings of organ crosstalk in AKI and highlight the related molecular mechanisms. Moreover, their crosstalk involves inflammatory and immune responses, hemodynamic change, fluid homeostasis, hormone secretion, nerve reflex regulation, uremic toxin, and oxidative stress. Our review provides important clues for the intervention for AKI and investigates important therapeutic potential from a new perspective.
14
Sanches, Eduardo, Yohan van de Looij, Sadou Sow, Audrey Toulotte, Analina da Silva, Laura Modernell, and Stéphane Sizonenko. "Dose-Dependent Neuroprotective Effects of Bovine Lactoferrin Following Neonatal Hypoxia–Ischemia in the Immature Rat Brain." Nutrients 13, no. 11 (October 29, 2021): 3880. http://dx.doi.org/10.3390/nu13113880.
Full textAbstract:
Injuries to the developing brain due to hypoxia–ischemia (HI) are common causes of neurological disabilities in preterm babies. HI, with oxygen deprivation to the brain or reduced cerebral blood perfusion due to birth asphyxia, often leads to severe brain damage and sequelae. Injury mechanisms include glutamate excitotoxicity, oxidative stress, blood–brain barrier dysfunction, and exacerbated inflammation. Nutritional intervention is emerging as a therapeutic alternative to prevent and rescue brain from HI injury. Lactoferrin (Lf) is an iron-binding protein present in saliva, tears, and breast milk, which has been shown to have antioxidant, anti-inflammatory and anti-apoptotic properties when administered to mothers as a dietary supplement during pregnancy and/or lactation in preclinical studies of developmental brain injuries. However, despite Lf’s promising neuroprotective effects, there is no established dose. Here, we tested three different doses of dietary maternal Lf supplementation using the postnatal day 3 HI model and evaluated the acute neurochemical damage profile using 1H Magnetic Resonance Spectroscopy (MRS) and long-term microstructure alterations using advanced diffusion imaging (DTI/NODDI) allied to protein expression and histological analysis. Pregnant Wistar rats were fed either control diet or bovine Lf supplemented chow at 0.1, 1, or 10 g/kg/body weight concentration from the last day of pregnancy (embryonic day 21–E21) to weaning. At postnatal day 3 (P3), pups from both sexes had their right common carotid artery permanently occluded and were exposed to 6% oxygen for 30 min. Sham rats had the incision but neither surgery nor hypoxia episode. At P4, MRS was performed on a 9.4 T scanner to obtain the neurochemical profile in the cortex. At P4 and P25, histological analysis and protein expression were assessed in the cortex and hippocampus. Brain volumes and ex vivo microstructural analysis using DTI/NODDI parameters were performed at P25. Acute metabolic disturbance induced in cortical tissue by HIP3 was reversed with all three doses of Lf. However, data obtained from MRS show that Lf neuroprotective effects were modulated by the dose. Through western blotting analysis, we observed that HI pups supplemented with Lf at 0.1 and 1 g/kg were able to counteract glutamatergic excitotoxicity and prevent metabolic failure. When 10 g/kg was administered, we observed reduced brain volumes, increased astrogliosis, and hypomyelination, pointing to detrimental effects of high Lf dose. In conclusion, Lf supplementation attenuates, in a dose-dependent manner, the acute and long-term cerebral injury caused by HI. Lf reached its optimal effects at a dose of 1 g/kg, which pinpoints the need to better understand effects of Lf, the pathways involved and possible harmful effects. These new data reinforce our knowledge regarding neuroprotection in developmental brain injury using Lf through lactation and provide new insights into lactoferrin’s neuroprotection capacities and limitation for immature brains.
15
Rakshit, Samrat, Satendra K. Nirala, and Monika Bhadauria. "Gallic Acid Protects from Acute Multiorgan Injury Induced by Lipopolysaccharide and D-galactosamine." Current Pharmaceutical Biotechnology 21, no. 14 (December 7, 2020): 1489–504. http://dx.doi.org/10.2174/1389201021666200615165732.
Full textAbstract:
Background: Secondary metabolites of plants, the polyphenols, play a vital role in protection from many health problems in human beings. Structurally favored phytochemicals may be studied to protect multiorgan injury. At pharmacological doses, gallic acid is nontoxic to mammals and is generally absorbed in the intestine. Aims: In this present study, gallic acid was evaluated for its protective efficacy against Lipo Polysaccharide (LPS) and d-Galactosamine (D-GalN) induced multiorgan injury, i.e., liver, kidney and brain. Methods: Three different doses of gallic acid (5, 10 and 20 mg/kg p.o.) were administered to the experimental animals for 6 consecutive days, followed by exposure to LPS (50 μg/kg I.P.) and D-GalN (300 mg/kg I.P.) on the 6th day. Discussion: Exposure to LPS and D-GalN severely increased lipid peroxidation, CYP2E1 activity and tissue lipids while lowered protein content. Gallic acid restored all these parameters towards control in dose dependent manner and 20 mg/kg dose provided the best protection. Histological study showed improved histoarchitecture of liver, kidney and brain that supported biochemical endpoints. Results: Exposure to LPS and D-GalN resulted in increased oxidative stress and proinflammatory cytokines. Altered hematology and serology due to LPS and D-GalN were restored towards control by gallic acid. Declined antioxidants such as reduced glutathione, superoxide dismutase and catalase due to injurious effects of LPS and D-GalN were rejuvenated by gallic acid. Conclusion: Gallic acid minimized oxidative stress and provided best protection at 20 mg/kg dose against LPS and D-GalN induced multi organ acute injury.
16
Yang, Xiaobo, Xiuying Li, Chuanhong Zhong, Jianhua Peng, Jinwei Pang, Tangming Peng, Weifeng Wan, and Xianglong Li. "Circular RNA circPHKA2 Relieves OGD-Induced Human Brain Microvascular Endothelial Cell Injuries through Competitively Binding miR-574-5p to Modulate SOD2." Oxidative Medicine and Cellular Longevity 2021 (November 8, 2021): 1–17. http://dx.doi.org/10.1155/2021/3823122.
Full textAbstract:
Background. Circular RNA phosphorylase kinase regulatory subunit alpha 2 (circPHKA2; hsa_circ_0090002) has a significantly, specifically different expression in acute ischemic stroke (AIS) patients’ blood. Here, we intended to investigate the role and mechanism of circPHKA2 in oxygen-glucose deprivation- (OGD-) induced stoke model in human brain microvascular endothelial cells (HBMEC). Methods. Expression of circPHKA2, microRNA- (miR-) 574-5p, and superoxide dismutase-2 (SOD2) was detected by quantitative PCR and western blotting. Cell injury was measured by detecting cell proliferation (EdU assay and CCK-8 assay), migration (transwell assay), neovascularization (tube formation assay), apoptosis (flow cytometry and western blotting), endoplasmic reticulum stress (western blotting), and oxidative stress (assay kits). Direct intermolecular interaction was determined by bioinformatics algorithms, dual-luciferase reporter assay, biotin-labelled miRNA capture, and argonaute 2 RNA immunoprecipitation. Results. circPHKA2 was downregulated in AIS patients’ blood in SOD2-correlated manner. Reexpressing circPHKA2 rescued EdU incorporation, cell viability and migration, tube formation, B cell lymphoma-2 (Bcl-2) expression, and SOD activity of OGD-induced HBMEC and alleviate apoptotic rate and levels of Bcl-2-associated protein (Bax), glucose-regulated protein 78 kD (GRP78), C/EBP-homologous protein (CHOP), caspase-12, reactive oxygen species (ROS), and malondialdehyde (MDA). Additionally, blocking SOD2 partially attenuated these roles of circPHKA2 overexpression. Molecularly, circPHKA2 upregulated SOD2 expression via interacting with miR-574-5p, and miR-574-5p could target SOD2. Similarly, allied to neurovascular protection of circPHKA2 was the downregulation of miR-574-5p. Conclusion. circPHKA2 could protect HBMEC against OGD-induced cerebral stroke model via the miR-574-5p/SOD2 axis, suggesting circPHKA2 as a novel and promising candidate in ischemic brain injury.
17
Shantanova, Larisa N., Daniil N. Olennikov, Irinchey E. Matkhanov, Sergey M. Gulyaev, Anyuta A. Toropova, Irina G. Nikolaeva, and Sergey M. Nikolaev. "Rhaponticum uniflorum and Serratula centauroides Extracts Attenuate Emotional Injury in Acute and Chronic Emotional Stress." Pharmaceuticals 14, no. 11 (November 19, 2021): 1186. http://dx.doi.org/10.3390/ph14111186.
Full textAbstract:
In modern life, the use of plant stress-protectors has taken on particular significance due to the wide distribution of neurosis-like and neurotic diseases caused by neuroendocrine-immune system imbalance. Special attention has been paid to the plants containing ecdysteroids, i.e., hormone-like bioactive substances with high adaptogenic activity. The article deals with the study of bioactivity of two plant extracts as Rhaponticum uniflorum (L.) DC. and Serratula centauroides L. with a high content of ecdysteroids and phenolic compounds. The models of acute and chronic emotional stress in white rats were used to estimate the stress-protective activity of R. uniflorum and S. centauroides extracts. Both extracts showed the stress-protective effect via inhibiting the development of signs induced by single and long-term effects of stress factors. In acute stress, the development of Selye's triad signs was less pronounced against the background of the plant remedies introduction. In chronic stress, the extracts prevented the development of anxiety-depressive syndrome. Besides, R. uniflorum and S. centauroides extracts banned the development of stress-induced injuries in the brain cortex and had a neuroprotective effect on ischemia against chronic stress. The stress-protective effects of both plant extracts were based on a decrease of hyperactivation of the central stress-promoting systems (sympathoadrenal, hypothalamic-pituitary-adrenal) due to their GABA-mimetic effects. Peripheral mechanisms were connected with the inhibition of free radical oxidation processes and with an increase in the endogenous antioxidant system activity. Thus, R. uniflorum and S. centauroides extracts have a high potential to increase non-specific body resistance against acute and chronic emotional stress effects.
18
Carter, Jessica, Guiying Deng, David Wagner, and Paco Herson. "Lymphocytes rapidly infiltrate into the brain following cardiac arrest and cardiopulmonary resuscitation (CA/CPR) (CAM5P.246)." Journal of Immunology 192, no. 1_Supplement (May 1, 2014): 180.17. http://dx.doi.org/10.4049/jimmunol.192.supp.180.17.
Full textAbstract:
Abstract Isolated ischemic episodes, such as occurs with stroke, result in long-term neural damage. It is known that lymphocytes along with other immune cells infiltrate brain tissue promoting that process. During cardiac arrest, global ischemia then reperfusion occurs. Although inflammatory mechanisms have been linked to neuronal injury following global cerebral ischemia, the presence of infiltrating immune cells remains understudied. We examined the brains of mice at different time points after global cerebral ischemia induced by cardiac arrest and cardiopulmonary resuscitation (CA/CPR) and characterized the influx of lymphocytes into the injured brain. We observed that CA/CPR caused a rapid influx of lymphocytes within 3 hours of resuscitation that was maintained for the duration of our experiments. The large majority of infiltrating lymphocytes were CD4+ T cells that expressed the Th1 characteristic cytokines TNFα or INFγ. Of the CD4+ infiltrating cells, a large portion of them were also CD40+ (Th40). Brain injury models attribute much of the neural damage to microglia and subsequent oxidative stress. We found that the CA/CPR injury model was largely dependent upon T cells, and the lack of functional T cells in TCRα knockout mice significantly reduced neuronal injury. This data indicate that studies investigating the neuro-immune response after global cerebral ischemia should consider the role of infiltrating T cells in orchestrating the acute and sustained immune response.
19
Zhang, Yuan, Wanpeng Yu, Christopher Flynn, Wenguang Chang, Lei Zhang, Man Wang, Wanhong Zheng, and Peifeng Li. "Interplay between Gut Microbiota and NLRP3 Inflammasome in Intracerebral Hemorrhage." Nutrients 14, no. 24 (December 9, 2022): 5251. http://dx.doi.org/10.3390/nu14245251.
Full textAbstract:
The pathophysiological process of intracerebral hemorrhage (ICH) is very complex, involving various mechanisms such as apoptosis, oxidative stress and inflammation. As one of the key factors, the inflammatory response is responsible for the pathological process of acute brain injury and is associated with the prognosis of patients. Abnormal or dysregulated inflammatory responses after ICH can aggravate cell damage in the injured brain tissue. The NOD-like receptor family pyrin domain-containing 3 (NLRP3) inflammasome is a multiprotein complex distributed in the cytosol, which can be triggered by multiple signals. The NLRP3 inflammasome is activated after ICH, thus promoting neuroinflammation and aggravating brain edema. In addition, there is evidence that the gut microbiota is crucial in the activation of the NLRP3 inflammasome. The gut microbiota plays a key role in a variety of CNS disorders. Changes in the diversity and species of the gut microbiota affect neuroinflammation through the activation of the NLRP3 inflammasome and the release of inflammatory cytokines. In turn, the gut microbiota composition can be influenced by the activation of the NLRP3 inflammasome. Thereby, the regulation of the microbe–gut–brain axis via the NLRP3 inflammasome may serve as a novel idea for protecting against secondary brain injury (SBI) in ICH patients. Here, we review the recent evidence on the functions of the NLRP3 inflammasome and the gut microbiota in ICH, as well as their interactions, during the pathological process of ICH.
20
Ikonomidou, Chrysanthy. "Cerebrospinal Fluid Biomarkers in Childhood Leukemias." Cancers 13, no. 3 (January 24, 2021): 438. http://dx.doi.org/10.3390/cancers13030438.
Full textAbstract:
Involvement of the central nervous system (CNS) in childhood leukemias remains a major cause of treatment failures. Analysis of the cerebrospinal fluid constitutes the most important diagnostic pillar in the detection of CNS leukemia and relies primarily on cytological and flow-cytometry studies. With increasing survival rates, it has become clear that treatments for pediatric leukemias pose a toll on the developing brain, as they may cause acute toxicities and persistent neurocognitive deficits. Preclinical research has demonstrated that established and newer therapies can injure and even destroy neuronal and glial cells in the brain. Both passive and active cell death forms can result from DNA damage, oxidative stress, cytokine release, and acceleration of cell aging. In addition, chemotherapy agents may impair neurogenesis as well as the function, formation, and plasticity of synapses. Clinical studies show that neurocognitive toxicity of chemotherapy is greatest in younger children. This raises concerns that, in addition to injury, chemotherapy may also disrupt crucial developmental events resulting in impairment of the formation and efficiency of neuronal networks. This review presents an overview of studies demonstrating that cerebrospinal fluid biomarkers can be utilized in tracing both CNS disease and neurotoxicity of administered treatments in childhood leukemias.
21
Vestergaard, Mark Bitsch, Otto Mølby Henriksen, Ulrich Lindberg, Niels Jacob Aachmann-Andersen, Kristian Lisbjerg, Søren Just Christensen, Niels Vidiendal Olsen, Ian Law, Henrik Bo Wiberg Larsson, and Peter Rasmussen. "No evidence for direct effects of recombinant human erythropoietin on cerebral blood flow and metabolism in healthy humans." Journal of Applied Physiology 124, no. 4 (April 1, 2018): 1107–16. http://dx.doi.org/10.1152/japplphysiol.00869.2017.
Full textAbstract:
Erythropoietin (EPO) is expressed in human brain tissue, but its exact role is unknown. EPO may improve the efficiency of oxidative metabolism and has neuroprotective properties against hypoxic injuries in animal models. We aimed to investigate the effect of recombinant human EPO (rHuEPO) administration on healthy cerebral metabolism in humans during normoxia and during metabolic stress by inhalation of 10% O2hypoxic air. Twenty-four healthy men participated in a two-arm double-blind placebo-controlled trial. rHuEPO was administered as a low dose (5,000 IU) over 4 wk ( n = 12) or as a high dose (500 IU·kg body wt−1·day−1) for three consecutive days ( n = 12). Global cerebral blood flow (CBF) and metabolic rate of glucose (CMRglc) were measured with positron emission tomography. CBF, metabolic rate of oxygen ([Formula: see text]), and cerebral lactate concentration were measured by magnetic resonance imaging and spectroscopy. Low-dose treatment increased hemoglobin and was associated with a near-significant decrease in CBF during baseline normoxia. High-dose treatment caused no change in CBF. Neither treatment had an effect on normoxia CMRglc, [Formula: see text], or lactate concentration or an effect on the cerebral metabolic response to inhalation of hypoxic air. In conclusion, the study found no evidence for a direct effect of rHuEPO on cerebral metabolism.NEW & NOTEWORTHY We demonstrate with magnetic resonance imaging and positron emission tomography that administration of erythropoietin does not have a substantial direct effect on healthy human resting cerebral blood flow or effect on cerebral glucose and oxygen metabolism. Also, administration of erythropoietin did not have a direct effect on the metabolic response to acute hypoxic stress in healthy humans, and a suggested neuroprotective effect from erythropoietin is therefore likely not a direct effect of erythropoietin on cerebral metabolism.
22
Cui, Wenwen, Yuanyuan Hao, Mingye Wang, Qiuyan Zhang, Junmei Wang, Gang Wei, and Yunlong Hou. "Inhibition of Autophagy Facilitates XY03-EA-Mediated Neuroprotection against the Cerebral Ischemia/Reperfusion Injury in Rats." Oxidative Medicine and Cellular Longevity 2022 (March 30, 2022): 1–20. http://dx.doi.org/10.1155/2022/7013299.
Full textAbstract:
Objective. L-3-n-Butylphthalide (NBP) is used to treat moderate and severe acute ischemia stroke. A previous screening study indicates that XY03-EA, a novel derivative of NBP, is more potent than NBP in the oxyradical scavenging capacity. In this study, in vivo and in vitro ischemia/reperfusion (I/R) models were used to test whether the XY03-EA offered therapeutic benefits in the ischemic stroke and explore the underlying mechanism of action. Methods. For this purpose, behavioral scores, cerebral infarct volume, cerebral blood flow, oxidative stress levels, inflammatory factor expression, energy metabolism levels, and autophagy activation were estimated in the rat middle cerebral artery occlusion and reperfusion (MCAO/R) model. The nonhuman primate MCAO/R model was conducted to validate the therapeutic effect of XY03-EA applied for 3 weeks. The neurological deficit score (NDS) progression rate and the infarct volume were continuously recorded on days 3, 7, 14, and 21. The PC-12 cell OGD/R model was used to assess the cell survival rate, reactive oxygen species (ROS) levels, the expression of autophagy execution molecules, and the activation of autophagy-related signaling pathways. Results. XY03-EA decreased the cerebral injuries and NDS by increasing cerebral blood flow, improving brain energy metabolism, accelerating ROS clearance, suppressing inflammatory responses, and inhibiting autophagy in the MCAO/R model rats. In the nonhuman primate MCAO/R model, the treatment of XY03-EA for 3 weeks could significantly inhibit the NDS progression rate and indicate a positive trend to reduce the infarct volume in a dose-dependent way. Mechanistically, XY03-EA inhibited ROS-dependent autophagy activation and thereby protected the PC-12 cells from the autophagic cell death induced by OGD/R. Conclusions. In this study, we found that XY03-EA alleviated the cerebral I/R injuries in rats and nonhuman primates. Our results demonstrated that XY03-EA exerted neuroprotective effects against the ROS-mediated autophagic neurocyte death and had great potential for the treatment of ischemic stroke.
23
Jurcau, Anamaria, and Adriana Ioana Ardelean. "Oxidative Stress in Ischemia/Reperfusion Injuries following Acute Ischemic Stroke." Biomedicines 10, no. 3 (March 1, 2022): 574. http://dx.doi.org/10.3390/biomedicines10030574.
Full textAbstract:
Recanalization therapy is increasingly used in the treatment of acute ischemic stroke. However, in about one third of these patients, recanalization is followed by ischemia/reperfusion injuries, and clinically to worsening of the neurological status. Much research has focused on unraveling the involved mechanisms in order to prevent or efficiently treat these injuries. What we know so far is that oxidative stress and mitochondrial dysfunction are significantly involved in the pathogenesis of ischemia/reperfusion injury. However, despite promising results obtained in experimental research, clinical studies trying to interfere with the oxidative pathways have mostly failed. The current article discusses the main mechanisms leading to ischemia/reperfusion injuries, such as mitochondrial dysfunction, excitotoxicity, and oxidative stress, and reviews the clinical trials with antioxidant molecules highlighting recent developments and future strategies.
24
Radak, Djordje, Ivana Resanovic, and Esma R. Isenovic. "Link Between Oxidative Stress and Acute Brain Ischemia." Angiology 65, no. 8 (October 16, 2013): 667–76. http://dx.doi.org/10.1177/0003319713506516.
Full text
25
Piloni, Natacha E., Virginia Fermandez, Luis A. Videla, and Susana Puntarulo. "Acute iron overload and oxidative stress in brain." Toxicology 314, no. 1 (December 2013): 174–82. http://dx.doi.org/10.1016/j.tox.2013.09.015.
Full text
26
Poulet, Roberta, Maria T. Gentile, Carmine Vecchione, Maria Distaso, Alessandra Aretini, Luigi Fratta, Giovanni Russo, et al. "Acute Hypertension Induces Oxidative Stress in Brain Tissues." Journal of Cerebral Blood Flow & Metabolism 26, no. 2 (August 3, 2005): 253–62. http://dx.doi.org/10.1038/sj.jcbfm.9600188.
Full text
27
Gupta, Shivali, Jian-Jun Wen, and Nisha Jain Garg. "Oxidative Stress in Chagas Disease." Interdisciplinary Perspectives on Infectious Diseases 2009 (2009): 1–8. http://dx.doi.org/10.1155/2009/190354.
Full textAbstract:
There is growing evidence to suggest that chagasic myocardia are exposed to sustained oxidative stress induced injuries that may contribute to disease progression. Trypanosoma cruzi invasion- and replication-mediated cellular injuries and immune-mediated cytotoxic reactions are the common source of reactive oxygen species (ROS) during acute infection. Mitochondria are proposed to be the major source of ROS in chronic chagasic hearts. However, it has not been established yet, whether mitochondrial dysfunction is a causative factor in chagasic cardiomyopathy or a consequence of other pathological events. A better understanding of oxidative stress in relation to cardiac tissue damage would be useful in the evaluation of its true role in the pathogenesis of Chagas disease and other heart diseases. In this review, we discuss the evidence for increased oxidative stress in chagasic disease, with emphasis on mitochondrial abnormalities, and its role in sustaining oxidative stress in myocardium.
28
Komsiyska, D. "Oxidative stress and post-stroke depression." Trakia Journal of Sciences 16, no. 3 (2018): 249–53. http://dx.doi.org/10.15547/tjs.2018.03.013.
Full textAbstract:
The topic of post-stroke depression etiology is reviewed in two main approaches. Some suggest that post-stroke depression is caused by the brain damage itself. On the contrary, others assume that this is a psychologic response to injuries or loss. Many discoveries can be examined as evidence for both the physiological and psychosocial mechanism of post-stroke depression. The two methods are not self-excluding, but instead describe post-stroke depression as a complex and multifactorial disease with interactions between the physiological and environmental factor. One hypothesis about depression occurrence is the inflammatory, oxidative and nitrosative stress (IO&NS) depression theory. Oxidative stress mechanisms are implied in the pathogenesis of mental diseases. The brain is considered particularly vulnerable to oxidative damage, due to its relatively high oxygen utilization and thus generation of free radical subordinate products, its modest antioxidant protections and its lipid-rich resistance.
29
Kovalčíková, Alexandra, Marianna Gyurászová, Diana Vavrincová-Yaghi, Peter Vavrinec, Ľubomíra Tóthová, Peter Boor, Katarína Šebeková, and Peter Celec. "Oxidative stress in the brain caused by acute kidney injury." Metabolic Brain Disease 33, no. 3 (March 7, 2018): 961–67. http://dx.doi.org/10.1007/s11011-018-0204-8.
Full text
30
Graham, Ernest M., O. P. Mishra, and Maria Delivoria-Papadopoulos. "Anti-oxidants and oxidative stress injuries to the brain in the perinatal period." Seminars in Neonatology 3, no. 2 (May 1998): 75–85. http://dx.doi.org/10.1016/s1084-2756(98)80025-0.
Full text
31
Dumitrescu, Laura, Iulia Popescu-Olaru, Liviu Cozma, Delia Tulbă, Mihail Eugen Hinescu, Laura Cristina Ceafalan, Mihaela Gherghiceanu, and Bogdan Ovidiu Popescu. "Oxidative Stress and the Microbiota-Gut-Brain Axis." Oxidative Medicine and Cellular Longevity 2018 (December 9, 2018): 1–12. http://dx.doi.org/10.1155/2018/2406594.
Full textAbstract:
The gut-brain axis is increasingly recognized as an important pathway of communication and of physiological regulation, and gut microbiota seems to play a significant role in this mutual relationship. Oxidative stress is one of the most important pathogenic mechanisms for both neurodegenerative diseases, such as Alzheimer’s or Parkinson’s, and acute conditions, such as stroke or traumatic brain injury. A peculiar microbiota type might increase brain inflammation and reactive oxygen species levels and might favor abnormal aggregation of proteins. Reversely, brain lesions of various etiologies result in alteration of gut properties and microbiota. These recent hypotheses could open a door for new therapeutic approaches in various neurological diseases.
32
Nakka, Venkata Prasuja, Phanithi Prakash-babu, and Raghu Vemuganti. "Crosstalk Between Endoplasmic Reticulum Stress, Oxidative Stress, and Autophagy: Potential Therapeutic Targets for Acute CNS Injuries." Molecular Neurobiology 53, no. 1 (December 9, 2014): 532–44. http://dx.doi.org/10.1007/s12035-014-9029-6.
Full text
33
Scott, Susan R., Kanhaiya Singh, Qing Yu, Chandan K. Sen, and Meijing Wang. "Sex as Biological Variable in Cardiac Mitochondrial Bioenergetic Responses to Acute Stress." International Journal of Molecular Sciences 23, no. 16 (August 18, 2022): 9312. http://dx.doi.org/10.3390/ijms23169312.
Full textAbstract:
Cardiac dysfunction/damage following trauma, shock, sepsis, and ischemia impacts clinical outcomes. Acute inflammation and oxidative stress triggered by these injuries impair mitochondria, which are critical to maintaining cardiac function. Despite sex dimorphisms in consequences of these injuries, it is unclear whether mitochondrial bioenergetic responses to inflammation/oxidative stress are sex-dependent. We hypothesized that sex disparity in mitochondrial bioenergetics following TNFα or H2O2 exposure is responsible for reported sex differences in cardiac damage/dysfunction. Methods and Results: Cardiomyocytes isolated from age-matched adult male and female mice were subjected to 1 h TNFα or H2O2 challenge, followed by detection of mitochondrial respiration capacity using the Seahorse XF96 Cell Mito Stress Test. Mitochondrial membrane potential (ΔΨm) was analyzed using JC-1 in TNFα-challenged cardiomyocytes. We found that cardiomyocytes isolated from female mice displayed a better mitochondrial bioenergetic response to TNFα or H2O2 than those isolated from male mice did. TNFα decreased ΔΨm in cardiomyocytes isolated from males but not from females. 17β-estradiol (E2) treatment improved mitochondrial metabolic function in cardiomyocytes from male mice subjected to TNFα or H2O2 treatment. Conclusions: Cardiomyocyte mitochondria from female mice were more resistant to acute stress than those from males. The female sex hormone E2 treatment protected cardiac mitochondria against acute inflammatory and oxidative stress.
34
Liao, Rick, Thomas R. Wood, and Elizabeth Nance. "Nanotherapeutic modulation of excitotoxicity and oxidative stress in acute brain injury." Nanobiomedicine 7 (January 1, 2020): 184954352097081. http://dx.doi.org/10.1177/1849543520970819.
Full textAbstract:
Excitotoxicity is a primary pathological process that occurs during stroke, traumatic brain injury (TBI), and global brain ischemia such as perinatal asphyxia. Excitotoxicity is triggered by an overabundance of excitatory neurotransmitters within the synapse, causing a detrimental cascade of excessive sodium and calcium influx, generation of reactive oxygen species, mitochondrial damage, and ultimately cell death. There are multiple potential points of intervention to combat excitotoxicity and downstream oxidative stress, yet there are currently no therapeutics clinically approved for this specific purpose. For a therapeutic to be effective against excitotoxicity, the therapeutic must accumulate at the disease site at the appropriate concentration at the right time. Nanotechnology can provide benefits for therapeutic delivery, including overcoming physiological obstacles such as the blood–brain barrier, protect cargo from degradation, and provide controlled release of a drug. This review evaluates the use of nano-based therapeutics to combat excitotoxicity in stroke, TBI, and hypoxia–ischemia with an emphasis on mitigating oxidative stress, and consideration of the path forward toward clinical translation.
35
Hao, Guangshan, Pinar Eser, and Jun Mo. "Oxidative Stress and Intracranial Hypertension after Aneurysmal Subarachnoid Hemorrhage." Antioxidants 11, no. 12 (December 8, 2022): 2423. http://dx.doi.org/10.3390/antiox11122423.
Full textAbstract:
Intracranial hypertension is a common phenomenon in patients with aneurysmal subarachnoid hemorrhage (aSAH). Elevated intracranial pressure (ICP) plays an important role in early brain injuries and is associated with unfavorable outcomes. Despite advances in the management of aSAH, there is no consensus about the mechanisms involved in ICP increases after aSAH. Recently, a growing body of evidence suggests that oxidative stress (OS) may play a crucial role in physio-pathological changes following aSAH, which may also contribute to increased ICP. Herein, we discuss a potential relation between increased ICP and OS, and resultantly propose antioxidant mechanisms as a potential therapeutic strategy for the treatment of ICP elevation following aSAH.
36
Liu, Jiankang, Helen C. Yeo, Eva Övervik-Douki, Tory Hagen, Stephanie J. Doniger, Daniel W. Chu, George A. Brooks, and Bruce N. Ames. "Chronically and acutely exercised rats: biomarkers of oxidative stress and endogenous antioxidants." Journal of Applied Physiology 89, no. 1 (July 1, 2000): 21–28. http://dx.doi.org/10.1152/jappl.2000.89.1.21.
Full textAbstract:
The responses to oxidative stress induced by chronic exercise (8-wk treadmill running) or acute exercise (treadmill running to exhaustion) were investigated in the brain, liver, heart, kidney, and muscles of rats. Various biomarkers of oxidative stress were measured, namely, lipid peroxidation [malondialdehyde (MDA)], protein oxidation (protein carbonyl levels and glutamine synthetase activity), oxidative DNA damage (8-hydroxy-2′-deoxyguanosine), and endogenous antioxidants (ascorbic acid, α-tocopherol, glutathione, ubiquinone, ubiquinol, and cysteine). The predominant changes are in MDA, ascorbic acid, glutathione, cysteine, and cystine. The mitochondrial fraction of brain and liver showed oxidative changes as assayed by MDA similar to those of the tissue homogenate. Our results show that the responses of the brain to oxidative stress by acute or chronic exercise are quite different from those in the liver, heart, fast muscle, and slow muscle; oxidative stress by acute or chronic exercise elicits different responses depending on the organ tissue type and its endogenous antioxidant levels.
37
Abdel-Salam, Omar M. E., Eman R. Youness, Fatma A. Morsy, and Amany Ameen Sleem. "Methylene Blue Protects Against Acute Ethanol-Induced Oxidative Stress and Organ Damage." International Journal of Halal Research 3, no. 2 (September 26, 2021): 88–102. http://dx.doi.org/10.18517/ijhr.3.2.88-102.2021.
Full textAbstract:
Ethanol (EtOH) intake is an important global health problem which affects many organs such as the brain, liver and stomach. The aim of the study was to examine the effect of the redox dye methylene blue (MethyB) on oxidative stress and histologic damage to the liver, gastric mucosa, and brain induced high dose ethanol (EtOH). Male rats were treated with EtOH (2 ml/rat, 96%) via intragastric route (for two consecutive days). MethyB (20 or 40 mg/kg, intraperitoneally) was given immediately after EtOH administration. The control group received saline. Rats were euthanized three hours after the last treatment. Brain and liver levels of malondialdehyde (MDA), reduced glutathione (GSH), and paraoxonase-1 (PON-1) as well as brain 5-lipoxygenase (5-LOX) and butyrylcholinesterase (BChE) were determined. Histopathological assessment of brain, liver and gastric damage was done. Results indicated that compared to saline treated animals, EtOH caused significant increase in MDA, along with decreased GSH and PON-1 activity in brain and liver. Additionally, it significantly increased 5-LOX and decreased brain BChE activity. The EtOH group showed the presence of dead and red neurons, and damage of glial cells. The liver exhibited vacuolar degeneration, apoptotic hepatocytes and foci of necrosis. The gastric mucosa showed areas of tissue damage, mucosal atrophy, and loss of normal architecture of glandular cells. The EtOH induced biochemical and histopathological alterations were alleviated after treatment with MethyB at a dose-dependent manner. These results demonstrate that MethyB is able to protect against from acute effects of EtOH on brain, liver and gastric tissue via an antioxidant action. MethyB might be of value in reducing tissue injury in acute EtOH intoxication.
38
Kerforne, Thomas, Sébastien Giraud, Jérôme Danion, Raphael Thuillier, Pierre Couturier, William Hebrard, Olivier Mimoz, and Thierry Hauet. "Rapid or Slow Time to Brain Death? Impact on Kidney Graft Injuries in an Allotransplantation Porcine Model." International Journal of Molecular Sciences 20, no. 15 (July 26, 2019): 3671. http://dx.doi.org/10.3390/ijms20153671.
Full textAbstract:
The use of donors deceased after brain death (DBD) with extended criteria in response to the shortage of grafts leads to the removal of more fragile kidneys. These grafts are at greater risk of not being grafted or delayed function. A better knowledge of the pathophysiology of DBDs would improve this situation. There is a difference between the results from animal models of DBD and the clinical data potentially explained by the kinetics of brain death induction. We compared the effect of the induction rate of brain death on the recovery of post-transplant renal function in a pig model of DBD followed by allografts in nephrectomized pigs. Resumption of early function post-transplant was better in the rapidly generated brain death group (RgBD) and graft fibrosis at three months less important. Two groups had identical oxidative stress intensity but a greater response to this oxidative stress by SIRT1, PGC1-α and NRF2 in the RgBD group. Modulation of mechanistic target of rapamycin (mTOR) stimulation by NRF2 would also regulate the survival/apoptosis balance of renal cells. For the first time we have shown that an allostatic response to oxidative stress can explain the impact of the rapidity of brain death induction on the quality of kidney transplants.
39
Lui, Pauline Po Yee, Xing Zhang, Shiyi Yao, Haonan Sun, and Caihao Huang. "Roles of Oxidative Stress in Acute Tendon Injury and Degenerative Tendinopathy—A Target for Intervention." International Journal of Molecular Sciences 23, no. 7 (March 25, 2022): 3571. http://dx.doi.org/10.3390/ijms23073571.
Full textAbstract:
Both acute and chronic tendon injuries are disabling sports medicine problems with no effective treatment at present. Sustained oxidative stress has been suggested as the major factor contributing to fibrosis and adhesion after acute tendon injury as well as pathological changes of degenerative tendinopathy. Numerous in vitro and in vivo studies have shown that the inhibition of oxidative stress can promote the tenogenic differentiation of tendon stem/progenitor cells, reduce tissue fibrosis and augment tendon repair. This review aims to systematically review the literature and summarize the clinical and pre-clinical evidence about the potential relationship of oxidative stress and tendon disorders. The literature in PubMed was searched using appropriate keywords. A total of 81 original pre-clinical and clinical articles directly related to the effects of oxidative stress and the activators or inhibitors of oxidative stress on the tendon were reviewed and included in this review article. The potential sources and mechanisms of oxidative stress in these debilitating tendon disorders is summarized. The anti-oxidative therapies that have been examined in the clinical and pre-clinical settings to reduce tendon fibrosis and adhesion or promote healing in tendinopathy are reviewed. The future research direction is also discussed.
40
Wakisaka, Yoshinobu, Yi Chu, Jordan D. Miller, Gary A. Rosenberg, and Donald D. Heistad. "Spontaneous Intracerebral Hemorrhage during Acute and Chronic Hypertension in Mice." Journal of Cerebral Blood Flow & Metabolism 30, no. 1 (September 2, 2009): 56–69. http://dx.doi.org/10.1038/jcbfm.2009.183.
Full textAbstract:
Oxidative stress and matrix metalloproteinases (MMPs) contribute to hemorrhagic transformation after ischemic stroke and brain injury after intracerebral hemorrhage (ICH). The goal of this study was to develop a new model of spontaneous ICH, based on the hypothesis that acute, superimposed on chronic, hypertension produces ICH. We hypothesized that increases in angiotensin II (AngII)-mediated oxidative stress and activation of MMPs are associated with, and may precede, spontaneous ICH during hypertension. In C57BL/6 mice, chronic hypertension was produced with AngII infusion and an inhibitor of nitric oxide synthase. During chronic hypertension, mice with acute hypertension from injections of AngII developed ICH. Oxidative stress and MMP levels increased in the brain even before developing ICH. Active MMPs colocalized with a marker of oxidative stress, especially on cerebral vessels that appeared to lead toward regions with ICH. Incidence of ICH and levels of oxidative stress and MMP-9 were greater in mice with acute hypertension produced by AngII than by norepinephrine. In summary, we have developed an experimental model of ICH during hypertension that may facilitate studies in genetically altered mice. We speculate that acute hypertension, especially when induced by AngII, may be critical in spontaneous ICH during chronic hypertension, possibly through oxidative stress and MMP-9.
41
Luca, Loredana, Alexandru Florin Rogobete, and Ovidiu Horea Bedreag. "Oxidative Stress and Antioxidant Therapy in Critically Ill Polytrauma Patients with Severe Head Injury." Journal of Critical Care Medicine 1, no. 3 (May 1, 2015): 83–91. http://dx.doi.org/10.1515/jccm-2015-0014.
Full textAbstract:
Abstract Traumatic Brain Injury (TBI) is one of the leading causes of death among critically ill patients from the Intensive Care Units (ICU). After primary traumatic injuries, secondary complications occur, which are responsible for the progressive degradation of the clinical status in this type of patients. These include severe inflammation, biochemical and physiological imbalances and disruption of the cellular functionality. The redox cellular potential is determined by the oxidant/antioxidant ratio. Redox potential is disturbed in case of TBI leading to oxidative stress (OS). A series of agression factors that accumulate after primary traumatic injuries lead to secondary lesions represented by brain ischemia and hypoxia, inflammatory and metabolic factors, coagulopathy, microvascular damage, neurotransmitter accumulation, blood-brain barrier disruption, excitotoxic damage, blood-spinal cord barrier damage, and mitochondrial dysfunctions. A cascade of pathophysiological events lead to accelerated production of free radicals (FR) that further sustain the OS. To minimize the OS and restore normal oxidant/antioxidant ratio, a series of antioxidant substances is recommended to be administrated (vitamin C, vitamin E, resveratrol, N-acetylcysteine). In this paper we present the biochemical and pathophysiological mechanism of action of FR in patients with TBI and the antioxidant therapy available.
42
Simic, Ivan, and Zivorad Malicevic. "The acute effects of 3,4-methylenedioxymethamphetamine on oxidative stress in rat brain." Medical review 61, no. 5-6 (2008): 222–25. http://dx.doi.org/10.2298/mpns0806222s.
Full textAbstract:
Introduction Oxidative stress and oxygen free radicals are thought to play an important role in acute effects of a number of neurotoxic processes. 3,4-Methylenedioxymethamphetamine (MDMA, ecstasy), a ring substituted amphetamine derivate, has attracted a great deal of media attention in recent years due to its widespread abuse as recreational drug by the young generation. The aim of the present study was to evaluate the acute effects of 3,4-methylenedioxymethamphetamine on oxidative stress parameters (index of lipid peroxidation - ILP, superoxide radicals O2-, superoxide dismutase - SOD and glutathione - GSH) in frontal cortex, striatum and hippocampus in Wistar rats. Materials and methods The study included 40 male Wistar rats (200-250 g), housed 4 per cage having free access to food and water. MDMA was dissolved in distillated water and administered peroraly at 5, 10, 20 or 40 mg/kg. 8 hours following MDMA, the rats were killed by decapitation, their brains were rapidly removed and the brain structures were dissected out on ice and analyzed biochemically. Results Acute peroral administration of a single dose (5, 10, 20 and 40 mg/kg) resulted in increase of ILP, O2-, SOD and decrease of GSH. Conclusion The results obtained in the present study suggest that oxidative stress plays a crucial role in MDMA-induced neurotoxicity and that the mechanism of MDMA neurotoxycity may vary between brain regions.
43
Kapczinski, Flávio, Benício N. Frey, Ana C. Andreazza, Márcia Kauer-Sant'Anna, Ângelo B. M. Cunha, and Robert M. Post. "Increased oxidative stress as a mechanism for decreased BDNF levels in acute manic episodes." Revista Brasileira de Psiquiatria 30, no. 3 (September 2008): 243–45. http://dx.doi.org/10.1590/s1516-44462008000300011.
Full textAbstract:
OBJECTIVE AND METHOD: There is a growing amount of data indicating that alterations in brain-derived neurotrophic factor and increased oxidative stress may play a role in the pathophysiology of bipolar disorder. In light of recent evidence demonstrating that brain-derived neurotrophic factor levels are decreased in situations of increased oxidative stress, we have examined the correlation between serum thiobarbituric acid reactive substances, a measure of lipid peroxidation, and serum brain-derived neurotrophic factor levels in bipolar disorder patients during acute mania and in healthy controls. RESULTS: Serum thiobarbituric acid reactive substances and brain-derived neurotrophic factor levels were negatively correlated in bipolar disorder patients (r = -0.56; p = 0.001), whereas no significant correlation was observed in the control group.. CONCLUSION: These results suggest that alterations in oxidative status may be mechanistically associated with abnormal low levels of brain-derived neurotrophic factor observed in individuals with bipolar disorder.
44
Chen, Meng-Hsiang, Pei-Chin Chen, Cheng-Hsien Lu, Hsiu-Ling Chen, Yi-Ping Chao, Shau-Hsuan Li, Yi-Wen Chen, and Wei-Che Lin. "Plasma DNA Mediate Autonomic Dysfunctions and White Matter Injuries in Patients with Parkinson’s Disease." Oxidative Medicine and Cellular Longevity 2017 (2017): 1–10. http://dx.doi.org/10.1155/2017/7371403.
Full textAbstract:
Background. Cardiovascular autonomic dysfunction is well known in Parkinson’s disease (PD) presentation and it produces hypoperfusion of vital organs. The association between cardiovascular autonomic dysfunction and oxidative stress was examined in previous animal models. Oxidative stress and neuroinflammation were thought to have roles in PD pathogenesis. Owing to the relative low intrinsic antioxidative properties, brain white matter (WM) is vulnerable to the oxidative stress. This study is conducted to examine possible relationships by using a hypothesis-driven mediation model. Methods. Twenty-nine patients with PD and 26 healthy controls participated in this study, with complete examinations of cardiac autonomic parameters, plasma DNA level, and WM integrity. A single-level three-variable mediation model was used to investigate the possible relationships. Results. The elevated serum oxidative stress biomarkers include plasma nuclear DNA and mitochondrial DNA, and poorer cardiac autonomic parameters and multiple regional microstructural WM changes are demonstrated. Further mediation analysis shows that plasma nuclear DNA served as the mediators between poorer baroreflex sensitivity and mean diffusivity changes in cingulum. Conclusions. These results provide a possible pathophysiology for how the poor baroreflex sensitivity and higher oxidative stress adversely impacted the WM integrity. This model could provide us with a piece of the puzzle of the entire PD pathogenesis.
45
Gamal, Maha, Zainab Abdel Wahab, Mohamed Eshra, Laila Rashed, and Nivin Sharawy. "Comparative Neuroprotective Effects of Dexamethasone and Minocycline during Hepatic Encephalopathy." Neurology Research International 2014 (2014): 1–8. http://dx.doi.org/10.1155/2014/254683.
Full textAbstract:
Objective.Encephalopathy and brain edema are serious complications of acute liver injury and may lead to rapid death of patients. The present study was designed to investigate the role of the inflammatory mediators and oxidative stress in the cytotoxic brain oedema and the neuroprotective effects of both minocycline and dexamethasone.Methods.48 male albino rats were divided into 4 groups: control group, acute liver injury (ALI) group, minocycline pretreated ALI group, and dexamethasone pretreated ALI group. 24 hours after acute liver injury serum ammonia, liver enzymes, brain levels of heme oxygenase-1 gene, iNOS gene expression, nitrite/nitrate, and cytokines were measured. In addition, the grades of encephalopathy and brain water content were assessed.Results.ALI was associated with significant increases in all measured inflammatory mediators, oxidative stress, iNOS gene expression, and nitrite/nitrate. Both minocycline and dexamethasone significantly modulated the inflammatory changes and the oxidative/nitrosative stress associated with ALI. However, only minocycline but not dexamethasone significantly reduced the cytotoxic brain oedema.Conclusion.Both minocycline and dexamethasone could modulate inflammatory and oxidative changes observed in brain after ALI and could be novel preventative therapy for hepatic encephalopathy episodes.
46
Jelinek, Matyas, Michal Jurajda, and Kamil Duris. "Oxidative Stress in the Brain: Basic Concepts and Treatment Strategies in Stroke." Antioxidants 10, no. 12 (November 25, 2021): 1886. http://dx.doi.org/10.3390/antiox10121886.
Full textAbstract:
The production of free radicals is inevitably associated with metabolism and other enzymatic processes. Under physiological conditions, however, free radicals are effectively eliminated by numerous antioxidant mechanisms. Oxidative stress occurs due to an imbalance between the production and elimination of free radicals under pathological conditions. Oxidative stress is also associated with ageing. The brain is prone to oxidative damage because of its high metabolic activity and high vulnerability to ischemic damage. Oxidative stress, thus, plays a major role in the pathophysiology of both acute and chronic pathologies in the brain, such as stroke, traumatic brain injury or neurodegenerative diseases. The goal of this article is to summarize the basic concepts of oxidative stress and its significance in brain pathologies, as well as to discuss treatment strategies for dealing with oxidative stress in stroke.
47
Lin, Wei-Ming, Meng-Hsiang Chen, Hung-Chen Wang, Cheng-Hsien Lu, Pei-Chin Chen, Hsiu-Ling Chen, Nai-Wen Tsai, et al. "Association between Peripheral Oxidative Stress and White Matter Damage in Acute Traumatic Brain Injury." BioMed Research International 2014 (2014): 1–8. http://dx.doi.org/10.1155/2014/340936.
Full textAbstract:
The oxidative stress is believed to be one of the mechanisms involved in the neuronal damage after acute traumatic brain injury (TBI). However, the disease severity correlation between oxidative stress biomarker level and deep brain microstructural changes in acute TBI remains unknown. In present study, twenty-four patients with acute TBI and 24 healthy volunteers underwent DTI. The peripheral blood oxidative biomarkers, like serum thiol and thiobarbituric acid-reactive substances (TBARS) concentrations, were also obtained. The DTI metrics of the deep brain regions, as well as the fractional anisotropy (FA) and apparent diffusion coefficient, were measured and correlated with disease severity, serum thiol, and TBARS levels. We found that patients with TBI displayed lower FAs in deep brain regions with abundant WMs and further correlated with increased serum TBARS level. Our study has shown a level of anatomic detail to the relationship between white matter (WM) damage and increased systemic oxidative stress in TBI which suggests common inflammatory processes that covary in both the peripheral and central reactions after TBI.
48
Orellana-Urzúa, Sofía, Ignacio Rojas, Lucas Líbano, and Ramón Rodrigo. "Pathophysiology of Ischemic Stroke: Role of Oxidative Stress." Current Pharmaceutical Design 26, no. 34 (October 13, 2020): 4246–60. http://dx.doi.org/10.2174/1381612826666200708133912.
Full textAbstract:
Stroke is the second leading cause of mortality and the major cause of adult physical disability worldwide. The currently available treatment to recanalize the blood flow in acute ischemic stroke is intravenous administration of tissue plasminogen activator (t-PA) and endovascular treatment. Nevertheless, those treatments have the disadvantage that reperfusion leads to a highly harmful reactive oxygen species (ROS) production, generating oxidative stress (OS), which is responsible for most of the ischemia-reperfusion injury and thus causing brain tissue damage. In addition, OS can lead brain cells to apoptosis, autophagy and necrosis. The aims of this review are to provide an updated overview of the role of OS in brain IRI, providing some bases for therapeutic interventions based on counteracting the OS-related mechanism of injury and thus suggesting novel possible strategies in the prevention of IRI after stroke.
49
Hu, Xiaoyan, Yanping Wang, Weihong Du, Li-Jun Liang, Wei Wang, and Xinchun Jin. "Role of Glial Cell-Derived Oxidative Stress in Blood-Brain Barrier Damage after Acute Ischemic Stroke." Oxidative Medicine and Cellular Longevity 2022 (September 2, 2022): 1–14. http://dx.doi.org/10.1155/2022/7762078.
Full textAbstract:
The integrity of the blood-brain barrier (BBB) is mainly maintained by endothelial cells and basement membrane and could be regulated by pericytes, neurons, and glial cells including astrocytes, microglia, oligodendrocytes (OLs), and oligodendrocyte progenitor cells (OPCs). BBB damage is the main pathological basis of hemorrhage transformation (HT) and vasogenic edema after stroke. In addition, BBB damage-induced HT and vasogenic edema will aggravate the secondary brain tissue damage. Of note, after reperfusion, oxidative stress-initiated cascade plays a critical role in the BBB damage after acute ischemic stroke (AIS). Although endothelial cells are the target of oxidative stress, the role of glial cell-derived oxidative stress in BBB damage after AIS also should receive more attention. In the current review, we first introduce the physiology and pathophysiology of the BBB, then we summarize the possible mechanisms related to BBB damage after AIS. We aim to characterize the role of glial cell-derived oxidative stress in BBB damage after AIS and discuss the role of oxidative stress in astrocytes, microglia cells and oligodendrocytes in after AIS, respectively.
50
Bramlett, Helen M., and W. Dalton Dietrich. "Pathophysiology of Cerebral Ischemia and Brain Trauma: Similarities and Differences." Journal of Cerebral Blood Flow & Metabolism 24, no. 2 (February 2004): 133–50. http://dx.doi.org/10.1097/01.wcb.0000111614.19196.04.
Full textAbstract:
Current knowledge regarding the pathophysiology of cerebral ischemia and brain trauma indicates that similar mechanisms contribute to loss of cellular integrity and tissue destruction. Mechanisms of cell damage include excitotoxicity, oxidative stress, free radical production, apoptosis and inflammation. Genetic and gender factors have also been shown to be important mediators of pathomechanisms present in both injury settings. However, the fact that these injuries arise from different types of primary insults leads to diverse cellular vulnerability patterns as well as a spectrum of injury processes. Blunt head trauma produces shear forces that result in primary membrane damage to neuronal cell bodies, white matter structures and vascular beds as well as secondary injury mechanisms. Severe cerebral ischemic insults lead to metabolic stress, ionic perturbations, and a complex cascade of biochemical and molecular events ultimately causing neuronal death. Similarities in the pathogenesis of these cerebral injuries may indicate that therapeutic strategies protective following ischemia may also be beneficial after trauma. This review summarizes and contrasts injury mechanisms after ischemia and trauma and discusses neuroprotective strategies that target both types of injuries.