scholarly journals Peran Ferritin pada Stroke Iskemik Akut

2021 ◽  
Vol 10 (2) ◽  
pp. 127-132
Author(s):  
Lisda Amalia ◽  
Keyword(s):  
Oxidative Stress ◽  
Ischemic Stroke ◽  
Iron Homeostasis ◽  
Cell Damage ◽  
The Body ◽  
Neurological Deficits ◽  
Iron Storage ◽  
The Central Nervous System ◽  
Focal Injury ◽  
Iron Storage Protein

Stroke is a neurological deficit that occurs due to acute focal injury to the central nervous system that occurs solely due to vascular disorders, including cerebral infarction or bleeding. Ferritin is an intracellular and extracellular iron storage protein which is essential for iron homeostasis in the body. Ferritin is expressed in microglia and macrophages, and also in neurons. If there is cell damage due to ischemic stroke, ferritin will leave the cells and enter the serum. The hypoxia-ischemic state in stroke induces the expression of ferritin in oligodendrocytes and microglia. When there is oxidative stress, ferritin formation will increase. The function of ferritin in times of oxidative stress is still controversial. Ferritin in this condition can act as a scavenger and as a donor for free iron ions. Ischemic stroke patients with larger lesions and more severe neurological deficits showed higher serum ferritin levels and a higher likelihood of complications of bleeding transformation.

scholarly journals Nimodipine Reappraised: An Old Drug With a Future

2019 ◽  
Vol 18 (1) ◽  
pp. 65-82 ◽  
Author(s):  
Andrew P. Carlson ◽  
Daniel Hänggi ◽  
Robert L. Macdonald ◽  
Claude W. Shuttleworth
Keyword(s):  
Ischemic Stroke ◽  
Aneurysmal Subarachnoid Hemorrhage ◽  
Clinical Care ◽  
Cell Types ◽  
Current Data ◽  
The Body ◽  
Neurological Deficits ◽  
Cerebral Vasoconstriction ◽  
Voltage Gated Calcium Channels ◽  
Dihydropyridine Calcium Channel Antagonist

Nimodipine is a dihydropyridine calcium channel antagonist that blocks the flux of extracellular calcium through L-type, voltage-gated calcium channels. While nimodipine is FDAapproved for the prevention and treatment of neurological deficits in patients with aneurysmal subarachnoid hemorrhage (aSAH), it affects myriad cell types throughout the body, and thus, likely has more complex mechanisms of action than simple inhibition of cerebral vasoconstriction. Newer understanding of the pathophysiology of delayed ischemic injury after a variety of acute neurologic injuries including aSAH, traumatic brain injury (TBI) and ischemic stroke, coupled with advances in the drug delivery method for nimodipine, have reignited interest in refining its potential therapeutic use. In this context, this review seeks to establish a firm understanding of current data on nimodipine’s role in the mechanisms of delayed injury in aSAH, TBI, and ischemic stroke, and assess the extensive clinical data evaluating its use in these conditions. In addition, we will review pivotal trials using locally administered, sustained release nimodipine and discuss why such an approach has evaded demonstration of efficacy, while seemingly having the potential to significantly improve clinical care.

scholarly journals Regulation of Iron Homeostasis and Related Diseases

2020 ◽  
Vol 2020 ◽  
pp. 1-11
Author(s):  
Yikun Li ◽  
Xiali Huang ◽  
Jingjing Wang ◽  
Ruiling Huang ◽  
Dan Wan
Keyword(s):  
Iron Homeostasis ◽  
Hereditary Hemochromatosis ◽  
Iron Concentration ◽  
Gene Mutations ◽  
The Body ◽  
Hereditary Diseases ◽  
Iron Regulation ◽  
Iron Storage ◽  
Smad Pathway ◽  
Infection And Inflammation

The liver is the organ for iron storage and regulation; it senses circulating iron concentrations in the body through the BMP-SMAD pathway and regulates the iron intake from food and erythrocyte recovery into the bloodstream by secreting hepcidin. Under iron deficiency, hypoxia, and hemorrhage, the liver reduces the expression of hepcidin to ensure the erythropoiesis but increases the excretion of hepcidin during infection and inflammation to reduce the usage of iron by pathogens. Excessive iron causes system iron overload; it accumulates in never system and damages neurocyte leading to neurodegenerative diseases such as Parkinson’s syndrome. When some gene mutations affect the perception of iron and iron regulation ability in the liver, then they decrease the expression of hepcidin, causing hereditary diseases such as hereditary hemochromatosis. This review summarizes the source and utilization of iron in the body, the liver regulates systemic iron homeostasis by sensing the circulating iron concentration, and the expression of hepcidin regulated by various signaling pathways, thereby understanding the pathogenesis of iron-related diseases.

scholarly journals Cell Envelope Perturbation Induces Oxidative Stress and Changes in Iron Homeostasis in Vibrio cholerae

2009 ◽  
Vol 191 (17) ◽  
pp. 5398-5408 ◽  
Author(s):  
Aleksandra E. Sikora ◽  
Sinem Beyhan ◽  
Michael Bagdasarian ◽  
Fitnat H. Yildiz ◽  
Maria Sandkvist
Keyword(s):  
Oxidative Stress ◽  
Gene Expression ◽  
Outer Membrane ◽  
Vibrio Cholerae ◽  
Iron Homeostasis ◽  
Cell Envelope ◽  
Membrane Integrity ◽  
Genetic Alterations ◽  
Iron Storage ◽  
Study Gene Expression

ABSTRACT The Vibrio cholerae type II secretion (T2S) machinery is a multiprotein complex that spans the cell envelope. When the T2S system is inactivated, cholera toxin and other exoproteins accumulate in the periplasmic compartment. Additionally, loss of secretion via the T2S system leads to a reduced growth rate, compromised outer membrane integrity, and induction of the extracytoplasmic stress factor RpoE (A. E. Sikora, S. R. Lybarger, and M. Sandkvist, J. Bacteriol. 189:8484-8495, 2007). In this study, gene expression profiling reveals that inactivation of the T2S system alters the expression of genes encoding cell envelope components and proteins involved in central metabolism, chemotaxis, motility, oxidative stress, and iron storage and acquisition. Consistent with the gene expression data, molecular and biochemical analyses indicate that the T2S mutants suffer from internal oxidative stress and increased levels of intracellular ferrous iron. By using a tolA mutant of V. cholerae that shares a similar compromised membrane phenotype but maintains a functional T2S machinery, we show that the formation of radical oxygen species, induction of oxidative stress, and changes in iron physiology are likely general responses to cell envelope damage and are not unique to T2S mutants. Finally, we demonstrate that disruption of the V. cholerae cell envelope by chemical treatment with polymyxin B similarly results in induction of the RpoE-mediated stress response, increased sensitivity to oxidants, and a change in iron metabolism. We propose that many types of extracytoplasmic stresses, caused either by genetic alterations of outer membrane constituents or by chemical or physical damage to the cell envelope, induce common signaling pathways that ultimately lead to internal oxidative stress and misregulation of iron homeostasis.

Serum ischemia-modified albumin levels in adolescent smokers

2016 ◽  
Vol 30 (1) ◽  
Author(s):  
Fatih Battal ◽  
Mustafa Tekin ◽  
Hakan Aylanç ◽  
Şule Yıldırım ◽  
Hakan Türkön ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cell Damage ◽  
The Body ◽  
Control Group ◽  
Negative Effects ◽  
Ischemia Modified Albumin ◽  
Tissue Ischemia ◽  
Adolescent Smokers ◽  
Significant Difference ◽  
Control Study

Abstract Background: It is known that the biochemical marker linked to tissue ischemia, ischemia-modified albumin (IMA), is related to oxidative stress. Cigarette smoking is a situation with increased oxidative stress causing cell damage and it is thought that many of the negative effects linked to smoking may occur after the biological material in the body is exposed to oxidative damage. This study aimed to identify variability in serum IMA levels in adolescents who smoke. Methods: This case-control study comprised 60 adolescents without any chronic disease. The smoking group was 30 adolescents between the ages of 14 and 17 years who smoked, while the control group was 30 healthy adolescents who did not smoke. Blood samples were collected from all subjects and serum IMA levels and serum nicotine metabolites were determined. Results: The serum IMA levels in the adolescents who smoked were 0.452±0.094 absorbance unit (ABSU), while the control group had ASBU levels of 0.427±0.054. There was no significant difference between the groups in terms of serum IMA levels (p=0.210). There was a significant difference between the control and smoking groups in terms of serum nicotine metabolite levels (p<0.001). Conclusions: Among adolescents who smoke, serum IMA levels may not be a good marker for oxidative stress.

scholarly journals Keratin-Based Epidermal Green Autofluorescence is a Common Biomarker of Organ Injury

2019 ◽  
Author(s):  
Mingchao Zhang ◽  
Yujia Li ◽  
Jiucun Wang ◽  
Huiru Tang ◽  
Zhong Yang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Lung Cancer ◽  
Ischemic Stroke ◽  
Recovery Phase ◽  
The Body ◽  
Organ Injury ◽  
Lung Cancer Patients ◽  
Non Invasive ◽  
And Oxidative Stress ◽  
Invasive Evaluation

AbstractIt is critical to discover biomarkers for non-invasive evaluation of the levels of inflammation and oxidative stress in human body - two key pathological factors in numerous diseases. Our study has indicated keratin 1-based epidermal autofluorescence (AF) as a biomarker of this type: Inducers of both inflammation and oxidative stress dose-dependently increased epidermal green AF with polyhedral structure in mice, with the AF intensity being highly associated with the dosages of the inducers. Lung cancer also induced increased epidermal green AF of mice, which was mediated by inflammation. Significant and asymmetrical increases in green AF intensity with polyhedral structure were found in the Dorsal Index Fingers’ skin of acute ischemic stroke (AIS) patients. While the AF intensity of the subjects with high risk for developing AIS, ischemic stroke patients in recovery phase and lung cancer patients was significantly higher than that of healthy controls, both AF intensity and AF asymmetry of these four groups were markedly lower than those of the AIS patients, which have shown promise for AIS diagnosis. Several lines of evidence have indicated K1 as an origin of the AF, e.g., K1 siRNA administration attenuated the oxidative stress-induced AF increase of mice. Collectively, our study has indicated K1-based epidermal AF as a biomarker for non-invasive evaluation of the levels of inflammation and oxidative stress in the body. These findings have established a basis for novel keratin’s AF-based biomedical imaging technology for non-invasive, efficient and economic diagnosis and screening of such inflammation- and oxidative stress-associated diseases as AIS.

scholarly journals Depleting SOX2 improves ischemic stroke via lncRNA PVT1/microRNA-24-3p/STAT3 axis

2021 ◽  
Vol 27 (1) ◽  
Author(s):  
Zhongjun Chen ◽  
Tieping Fan ◽  
Xusheng Zhao ◽  
Zhichen Zhang
Keyword(s):  
Oxidative Stress ◽  
Ischemic Stroke ◽  
Brain Injury ◽  
Water Content ◽  
Artery Occlusion ◽  
Neurological Deficits ◽  
Neuron Survival ◽  
Non Coding Rna ◽  
Cerebral Artery Occlusion ◽  
And Oxidative Stress

Abstract Objectives Studies have widely explored in the filed of ischemic stroke (IS) with their focus on transcription factors. However, few studies have pivoted on sex determining region Y-box 2 (SOX2) in IS. Thus, this study is launched to figure out the mechanisms of SOX2 in IS. Methods Rat middle cerebral artery occlusion (MCAO) was established as a stroke model. MCAO rats were injected with depleted SOX2 or long non-coding RNA plasmacytoma variant translocation 1 (PVT1) to explore their roles in neurological deficits, cerebral water content, neuron survival, apoptosis and oxidative stress. The relationship among SOX2, PVT1, microRNA (miR)-24-3p and signal transducer and activator of transcription 3 (STAT3) was verified by a series of experiments. Results SOX2, PVT1 and STAT3 were highly expressed while miR-24-3p was poorly expressed in cerebral cortex tissues of MCAO rats. Depleted SOX2 or PVT1 alleviated brain injury in MCAO rats as reflected by neuronal apoptosis and oxidative stress restriction, brain water content reduction, and neurological deficit and neuron survival improvements. Overexpression of PVT1 functioned oppositely. Restored miR-24-3p abolished PVT1 overexpression-induced brain injury in MCAO rats. SOX2 directly promoted PVT1 expression and further increased STAT3 by sponging miR-24-3p. Conclusion This study presents that depleting SOX2 improves IS via PVT1/miR-24-3p/STAT3 axis which may broaden our knowledge about the mechanisms of SOX2/PVT1/miR-24-3p/STAT3 axis and provide a reference of therapy for IS.

scholarly journals PerR Controls Oxidative Stress Resistance and Iron Storage Proteins and Is Required for Virulence in Staphylococcus aureus

2001 ◽  
Vol 69 (6) ◽  
pp. 3744-3754 ◽  
Author(s):  
Malcolm J. Horsburgh ◽  
Mark O. Clements ◽  
Howard Crossley ◽  
Eileen Ingham ◽  
Simon J. Foster
Keyword(s):  
Oxidative Stress ◽  
Staphylococcus Aureus ◽  
Stress Resistance ◽  
Iron Homeostasis ◽  
Storage Proteins ◽  
Iron Storage ◽  
Oxidative Stress Resistance ◽  
Genes Encoding ◽  
Starvation Survival ◽  
Iron Storage Proteins

ABSTRACT The Staphylococcus aureus genome encodes three ferric uptake regulator (Fur) homologues: Fur, PerR, and Zur. To determine the exact role of PerR, we inactivated the gene by allelic replacement using a kanamycin cassette, creating strain MJH001 (perR). PerR was found to control transcription of the genes encoding the oxidative stress resistance proteins catalase (KatA), alkyl hydroperoxide reductase (AhpCF), bacterioferritin comigratory protein (Bcp), and thioredoxin reductase (TrxB). Furthermore, PerR regulates transcription of the genes encoding the iron storage proteins ferritin (Ftn) and the ferritin-like Dps homologue, MrgA. Transcription of perR was autoregulated, and PerR repressed transcription of the iron homeostasis regulator Fur, which is a positive regulator of catalase expression. PerR functions as a manganese-dependent, transcriptional repressor of the identified regulon. Elevated iron concentrations produced induction of the PerR regulon. PerR may act as a peroxide sensor, since addition of external hydrogen peroxide to 8325-4 (wild type) resulted in increased transcription of most of the PerR regulon, except forfur and perR itself. The PerR-regulatedkatA gene encodes the sole catalase of S. aureus, which is an important starvation survival determinant but is surprisingly not required for pathogenicity in a murine skin abscess model of infection. In contrast, PerR is not necessary for starvation survival but is required for full virulence (P < 0.005) in this model of infection. PerR ofS. aureus may act as a redox sentinel protein during infection, analogous to the in vitro activities of OxyR and PerR ofEscherichia coli and Bacillus subtilis, respectively. However, it differs in its response to the metal balance within the cell and has the added capability of regulating iron uptake and storage.

scholarly journals Antioxidant Activity of Pigmented Rice and Impact on Health

JURNAL PANGAN ◽  
2019 ◽  
Vol 28 (1) ◽  
pp. 11-22
Author(s):  
Arfina Sukmawati Arifin
Keyword(s):  
Oxidative Stress ◽  
Diabetes Mellitus ◽  
Antioxidant Activity ◽  
Vascular Function ◽  
Healthy Lifestyle ◽  
Cell Damage ◽  
The Body ◽  
Food Sources

The high number of free radicals that are not balanced with the amount of antioxidants in the body triggers oxidative stress. Oxidative stress causes impaired vascular function, damage to proteins and lipids in membrane cell, and nucleic acid (DNA) mutations. Chronic cell damage has a negative effect on tissue that triggers various diseases such as neurodegenerative diseases (Alzheimer's, Parkinson's), cardiovascular diseases (hypertension, arteriosclerosis, and others), cataracts, retinal damage, maculopathy, rheumatoid arthritis, asthma, stroke, diabetes mellitus , immunodepression, cancer, aging, hyperoxia, dermatitis, and others. The application of a healthy lifestyle for example by consuming food sources of bioactive compounds can minimize health risks. Rice is the staple food of the Indonesian people. Some types of rice contain red and black pigments which are known to have high antioxidant activity compared to white rice. The pigment comes from anthocyanin and proanthocyanidin. Various studies in vitro and in vivo prove that anthocyanin and proantocyanidine act as antioxidants and potency as a preventative for various diseases such as cardiovascular, diabetes mellitus, and etc.

scholarly journals TNF-α Receptor Inhibitor Alleviates Metabolic and Inflammatory Changes in a Rat Model of Ischemic Stroke

Antioxidants ◽  
2021 ◽  
Vol 10 (6) ◽  
pp. 851
Author(s):  
Shih-Yi Lin ◽  
Ya-Yu Wang ◽  
Cheng-Yi Chang ◽  
Chih-Cheng Wu ◽  
Wen-Ying Chen ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Ischemic Stroke ◽  
Rat Model ◽  
Brain Infarction ◽  
In Vitro Study ◽  
Neurological Deficits ◽  
Tnf Α ◽  
Anti Inflammatory ◽  
Receptor Inhibitor

Hyperglycemia and inflammation, with their augmented interplay, are involved in cases of stroke with poor outcomes. Interrupting this vicious cycle thus has the potential to prevent stroke disease progression. Tumor necrosis factor-α (TNF-α) is an emerging molecule, which has inflammatory and metabolic roles. Studies have shown that TNF-α receptor inhibitor R-7050 possesses neuroprotective, antihyperglycemic, and anti-inflammatory effects. Using a rat model of permanent cerebral ischemia, pretreatment with R-7050 offered protection against poststroke neurological deficits, brain infarction, edema, oxidative stress, and caspase 3 activation. In the injured cortical tissues, R-7050 reversed the activation of TNF receptor-I (TNFRI), NF-κB, and interleukin-6 (IL-6), as well as the reduction of zonula occludens-1 (ZO-1). In the in vitro study on bEnd.3 endothelial cells, R-7050 reduced the decline of ZO-1 levels after TNF-α-exposure. R-7050 also reduced the metabolic alterations occurring after ischemic stroke, such as hyperglycemia and increased plasma corticosterone, free fatty acids, C reactive protein, and fibroblast growth factor-15 concentrations. In the gastrocnemius muscles of rats with stroke, R-7050 improved activated TNFRI/NF-κB, oxidative stress, and IL-6 pathways, as well as impaired insulin signaling. Overall, our findings highlight a feasible way to combat stroke disease based on an anti-TNF therapy that involves anti-inflammatory and metabolic mechanisms.

Effects of Vitamin C and E Against Oxidative Stress: Is Antioxidant Supplementation Efficient?

2020 ◽  
Vol 1 (1) ◽  
pp. 33-41
Author(s):  
Amel Saidi Merzouk ◽  
Bouchra Loukidi ◽  
Réda Bettioui ◽  
Hafida Merzouk
Keyword(s):  
Oxidative Stress ◽  
Vitamin C ◽  
Metabolic Diseases ◽  
Cell Damage ◽  
The Body ◽  
Antioxidant Supplementation ◽  
Negative Effects ◽  
Oxidation Stress ◽  
Antioxidant Supplements

Objective: Numerous epidemiological studies show an increased prevalence of metabolic diseases related to oxidation stress causing cell damage. Antioxidant supplementation is therefore useful to protect against the oxidative stress mediated disease development and has become an increasingly popular practice. In this review, a selection of clinical and in vitro studies on vitamin C and E supplementation and the evaluation of their beneficial or negative effects have been analyzed. Results: Clinical studies and supplementation trials show a correlation between antioxidants and metabolic improvement in different diseases such as cancer, cardiovascular disease, diabetes, obesity. Vitamin C (ascorbic acid) and E (α-tocopherol) appear to be among the most commonly used antioxidants. However, taking antioxidant supplements in high doses can be harmful. In some studies, little supportive evidence has been provided on substantial protection against chronic diseases by antioxidants. In addition, previous studies have revealed negative effects of antioxidant supplements such as pro-oxidant activities in particular conditions including their dosage and the body oxidant/ antioxidant status. Conclusion: Antioxidant supplements should be used with caution.

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