scholarly journals Oxidative Stress Biomarkers: Establishment of Reference Values for Isoprostanes, AOPP, and NPBI in Cord Blood

2017 ◽  
Vol 2017 ◽  
pp. 1-6 ◽  
Author(s):  
Mariangela Longini ◽  
Elisa Belvisi ◽  
Fabrizio Proietti ◽  
Francesco Bazzini ◽  
Giuseppe Buonocore ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Reference Values ◽  
Ischemia Reperfusion ◽  
Public Health Problem ◽  
Perinatal Period ◽  
Healthy Population ◽  
Oxidative Stress Biomarkers ◽  
Fenton Chemistry ◽  
Term Newborns

Oxidative stress (OS) is a common pathogenic factor involved in the onset of several diseases in humans, from immunologic disorders to malignancy, being a serious public health problem. In perinatal period, OS has been associated with adverse outcome of pregnancy and neonatal diseases. Dangerous effects of OS are mediated by increased production of free radicals (FRs) following various mechanisms, such as hypoxia, ischemia reperfusion, hyperoxia, inflammation, mitochondrial dysfunction, Fenton chemistry, and prostaglandin metabolism. FRs have short half-life, and their measurement in vivo is faced with many challenges. However, oxyradical derivatives are stable and thus may be measured and monitored repeatedly. The quantification of OS is based on the measurement of specific biomarkers in biologic fluids and tissues, which reflect induced oxidative damage to lipids, proteins, and DNA. Prostanoids, non–protein-bound iron (NPBI), and advanced oxidation protein products (AOPP) are actually considered truly specific and reliable for neonatal injury. Defining reference values for these biomarkers is necessary to investigate their role in neonatal diseases or also to evaluate the success of treatments. In this work, we wanted to define laboratory reference values for biomarkers of OS in a healthy population of term newborns.

scholarly journals Diallyl Trisulfide Protects Rat Brain Tissue against the Damage Induced by Ischemia-Reperfusion through the Nrf2 Pathway

Antioxidants ◽  
2019 ◽  
Vol 8 (9) ◽  
pp. 410 ◽  
Author(s):  
Carlos A. Silva-Islas ◽  
María E. Chánez-Cárdenas ◽  
Diana Barrera-Oviedo ◽  
Alma Ortiz-Plata ◽  
José Pedraza-Chaverri ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cerebral Ischemia ◽  
Protective Effect ◽  
Ischemia Reperfusion ◽  
Public Health Problem ◽  
Related Factor ◽  
Diallyl Trisulfide ◽  
In Vivo Models ◽  
Nrf2 Activation

Stroke is a public health problem due to its high mortality and disability rates; despite these, the pharmacological treatments are limited. Oxidative stress plays an important role in cerebral damage in stroke and the activation of the nuclear factor erythroid 2-related factor 2 (Nrf2) confers protection against oxidative stress. Different compounds, such as diallyl trisulfide (DATS), have the ability to activate Nrf2. DATS protects against the damage induced in oxygen-glucose deprivation in neuronal cells; however, in in vivo models of cerebral ischemia, DATS has not been evaluated. Male Wistar rats were subjected to 1 h of ischemia and seven days of reperfusion and the protective effect of DATS was evaluated. DATS administration (IR + DATS) decreased the infarct area and brain damage in the striatum and cortex; improved neurological function; decreased malondialdehyde and metalloproteinase-9 levels; increased Nrf2 activation in the cortex and the expression of superoxide dismutase 1 (SOD1) in the nucleus, SOD2 and glutathione S-transferase (GST) in the striatum and cortex; and increased the activity of catalase (CAT) in the striatum and glutathione peroxidase (GPx) in the cortex. Our results demonstrate the protective effect of DATS in an in vivo model of cerebral ischemia that involves Nrf2 activation.

Reference values of oxidative stress biomarkers in healthy newborns

2013 ◽  
Vol 55 (5) ◽  
pp. 604-607 ◽  
Author(s):  
Ahmet Akçay ◽  
Hatice Tatar Aksoy ◽  
Nurdan Uras ◽  
Uğur Dilmen
Keyword(s):  
Oxidative Stress ◽  
Reference Values ◽  
Oxidative Stress Biomarkers ◽  
Stress Biomarkers

Abstract P293: Endogenous Lats2 Plays an Important Role in Mediating Myocardial Injury Caused by Ischemia/Reperfusion Through Inhibition of FoxO3

2011 ◽  
Vol 109 (suppl_1) ◽  
Author(s):  
Dan Shao ◽  
Peiyong Zhai ◽  
Junichi Sadoshima
Keyword(s):  
Oxidative Stress ◽  
Myocardial Injury ◽  
Ischemia Reperfusion ◽  
Systolic Pressure ◽  
Left Ventricular ◽  
Dominant Negative ◽  
Area At Risk ◽  
Perfused Heart ◽  
Developed Pressure

Lats2 is a tumor suppressor and a serine/threonine kinase, acting downstream of mammalian sterile 20 like kinase1 (Mst1), which stimulates apoptosis and inhibits hypertrophy in cardiomyocytes (CM). We investigated the role of Lats2 in mediating myocardial injury after ischemia/reperfusion (IR). Phosphorylation of YAP, an in vivo substrate of Lats2, was increased after 45 minutes ischemia followed by 24 hours reperfusion in control mouse hearts compared with sham, but not in dominant negative (DN) Lats2 transgenic mouse (Tg) hearts, suggesting that Lats2 is activated by IR. The size of myocardial infarction (MI)/area at risk was significantly smaller in Tg mice than in NTg mice (19% and 49%, p<0.01). And there were fewer TUNEL positive cells in Tg than in NTg mice (0.04% and 0.11%, p<0.05). Following 30 min of global ischemia and 60 min of reperfusion in Langendorff perfused heart preparations, left ventricular (LV) systolic pressure (100 vs 71mmHg, p<0.05) and LV developed pressure (79 vs 47 mmHg, p<0.05) were significantly greater in Tg than in NTg mice, indicating that suppression of Lats2 induces better functional recovery after IR. Oxidative stress, as evaluated by 8-OHdG staining, was attenuated in Tg mice. In cultured CMs, DN-Lats2 significantly decreased H 2 O 2 -induced cell death. Overexpression of Lats2 significantly downregulated (51% and 75%, p<0.05), whereas that of DN-Last2 upregulated (100 and 70%, p<0.05), MnSOD and catalase, suggesting that Lats2 negatively regulates expression of antioxidants. Reporter gene assays showed that overexpression of Lats2 significantly inhibits (−70%), whereas knocking down Lats2 by sh-Lats2 increases (+60%), FoxO3-mediated transcriptional activity. Overexpression of Lats2 in CMs inhibited FoxO3 expression, whereas that of DN-Lats2 significantly inhibited FoxO3 downregulation after IR in vivo, suggesting that Lats2 negatively regulates FoxO3 protein expression, which may lead to the downregulation of MnSOD and catalase. Taken together, these results suggest that endogenous Lats2 plays an important role in mediating myocardial injury in response to IR, In part through downregulation of FoxO3 and consequent downregulation of antioxidants and increased oxidative stress in the heart.

scholarly journals Galangin Alleviates Liver Ischemia-Reperfusion Injury in a Rat Model by Mediating the PI3K/AKT Pathway

2018 ◽  
Vol 51 (3) ◽  
pp. 1354-1363 ◽  
Author(s):  
Yang Li ◽  
Liquan Tong ◽  
Jingyan Zhang ◽  
Yafeng Zhang ◽  
Feng  Zhang
Keyword(s):  
Oxidative Stress ◽  
Ischemia Reperfusion Injury ◽  
Hepatic Duct ◽  
Ischemia Reperfusion ◽  
Trauma Surgery ◽  
Liver Ischemia ◽  
Western Blots ◽  
Phosphorylated Akt ◽  
Related Proteins

Background/Aims: Liver ischemia-reperfusion (I/R) injury is a pathological process that often occurs during liver and trauma surgery. There are numerous causes of liver I/R injury, but the mechanism is unknown. Galangin (GA) is a flavonoid, a polyphenolic compound widely distributed in medicinal herbs that has anti-inflammatory, antioxidant, and antitumor activity. This study evaluated the protective effect of GA on hepatic I/R injury. Methods: An I/R model was created in male Wistar rats by clamping the hepatoportal vein, hepatic artery and hepatic duct for 30 min followed by reperfusion for 2 h. A hypoxia/restoration (H/R) model was established in buffalo rat liver (BRL) cells by hypoxia for 4 h followed by normoxic conditions for 10 h. The extent of liver injury was assayed by serum ALT/AST, hepatic histology, and MPO activity. Oxidative stress was assayed by serum superoxide dismutase (SOD), catalase (CAT), glutathione (GSH) and malondialdehyde (MDA). Expression of apoptosis-related proteins in BRL cells was assayed in western blots. Expression of AKT and p-AKT proteins in vivo and vitro were assayed in western blots. Results: GA significantly decreased ALT/AST expression, reversed changes in oxidative stress markers induced by I/R, and mediated caspase-3 activity expression of apoptosis-related proteins in vivo and in vitro. Methylthiazol tetrazolium (MTT) assay, flow cytometry, and Hoechst 33258 staining confirmed that GA inhibited apoptosis of BRL cells. GA also increased the expression of phosphorylated AKT after H/R. Conclusion: GA reduced liver I/R injury both in vivo and vitro and inhibited BRL cell apoptosis. PI3K/AKT signaling have been involved. GA may protect against liver I/R and be a potential therapeutic candidate.

scholarly journals Effect of sodium (S)-2-hydroxyglutarate in male, and succinic acid in female Wistar rats against renal ischemia-reperfusion injury, suggesting a role of the HIF-1 pathway

PeerJ ◽  
2020 ◽  
Vol 8 ◽  
pp. e9438
Author(s):  
Eduardo Cienfuegos-Pecina ◽  
Tannya R. Ibarra-Rivera ◽  
Alma L. Saucedo ◽  
Luis A. Ramírez-Martínez ◽  
Deanna Esquivel-Figueroa ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Succinic Acid ◽  
Wistar Rats ◽  
Ischemia Reperfusion ◽  
The Other ◽  
Oxidative Stress Biomarkers ◽  
Stress Biomarkers ◽  
Female Wistar Rats ◽  
Dose Dependent ◽  
Nephroprotective Effect

Background Ischemia–reperfusion (IR) injury is the main cause of delayed graft function in solid organ transplantation. Hypoxia-inducible factors (HIFs) control the expression of genes related to preconditioning against IR injury. During normoxia, HIF-α subunits are marked for degradation by the egg-laying defective nine homolog (EGLN) family of prolyl-4-hydroxylases. The inhibition of EGLN stabilizes HIFs and protects against IR injury. The aim of this study was to determine whether the EGLN inhibitors sodium (S)-2-hydroxyglutarate [(S)-2HG] and succinic acid (SA) have a nephroprotective effect against renal IR injury in Wistar rats. Methods (S)-2HG was synthesized in a 22.96% yield from commercially available L-glutamic acid in a two-step methodology (diazotization/alkaline hydrolysis), and its structure was confirmed by nuclear magnetic resonance and polarimetry. SA was acquired commercially. (S)-2HG and SA were independently evaluated in male and female Wistar rats respectively after renal IR injury. Rats were divided into the following groups: sham (SH), nontoxicity [(S)-2HG: 12.5 or 25 mg/kg; SA: 12.5, 25, or 50 mg/kg], IR, and compound+IR [(S)-2HG: 12.5 or 25 mg/kg; SA: 12.5, 25, or 50 mg/kg]; independent SH and IR groups were used for each assessed compound. Markers of kidney injury (BUN, creatinine, glucose, and uric acid) and liver function (ALT, AST, ALP, LDH, serum proteins, and albumin), proinflammatory cytokines (IL-1β, IL-6, and TNF-α), oxidative stress biomarkers (malondialdehyde and superoxide dismutase), and histological parameters (tubular necrosis, acidophilic casts, and vascular congestion) were assessed. Tissue HIF-1α was measured by ELISA and Western blot, and the expression of Hmox1 was assessed by RT-qPCR. Results (S)-2HG had a dose-dependent nephroprotective effect, as evidenced by a significant reduction in the changes in the BUN, creatinine, ALP, AST, and LDH levels compared with the IR group. Tissue HIF-1α was only increased in the IR group compared to SH; however, (S)-2HG caused a significant increase in the expression of Hmox1, suggesting an early accumulation of HIF-1α in the (S)-2HG-treated groups. There were no significant effects on the other biomarkers. SA did not show a nephroprotective effect; the only changes were a decrease in creatinine level at 12.5 mg/kg and increased IR injury at 50 mg/kg. There were no effects on the other biochemical, proinflammatory, or oxidative stress biomarkers. Conclusion None of the compounds were hepatotoxic at the tested doses. (S)-2HG showed a dose-dependent nephroprotective effect at the evaluated doses, which involved an increase in the expression of Hmox1, suggesting stabilization of HIF-1α. SA did not show a nephroprotective effect but tended to increase IR injury when given at high doses.

scholarly journals In vivo and In vitro Antioxidant Activities of Aqueous and Ethanol Stem Bark Extracts of Vitex doniana on Doxorubicin-induced Oxidative Stress in Rats

2021 ◽  
pp. 44-55
Author(s):  
Mohammed Aliyu Sulaiman ◽  
Daniel Dahiru ◽  
Mohammed Auwal Ibrahim ◽  
Ahmed Ibrahim Hayatu
Keyword(s):  
Oxidative Stress ◽  
Antioxidant Activities ◽  
Ischemia Reperfusion ◽  
Oral Treatment ◽  
Stem Bark ◽  
Albino Rats ◽  
Associated Diseases ◽  
Vitex Doniana

Background: Oxidative stress is involved in the pathogenesis of hypertension, myocardial ischemia-reperfusion injury, atherosclerosis, muscular dystrophy, aging and other associated diseases. Vitex doniana is used in Adamawa, northern Nigeria to treat oxidative stress associated diseases. However, the antioxidative effects of the plant have not been scientifically examined in oxidative stress experimental animal models. The aim of this study is to investigate the in vitro and in vivo antioxidant activities of aqueous and ethanol stem bark extracts of Vitex doniana in oxidative stress model of rats. Methods: The study used 35 adult albino rats weighing 175 ± 25 g, of which 30 were induced with oxidative stress by intraperitoneal injection of doxorubicin (10 mg/kg) for three consecutive days. Animals were treated by oral administration of silymarin (100 mg/kg) and Vitex doniana aqueous or ethanol extract (100 mg/kg and 200 mg/kg) for 14 consecutive days before they were sacrificed on the 15th day and blood was analyzed for biochemical indices of oxidative stress. Results: The results of the phytochemistry showed the presence of alkaloids, tannins, flavonoids, steroids, phenols, saponins, terpenoids, glycosides: and total flavonoids (52.70 ± 1.60 mg/ml and 75.40 ± 0.80 mg/ml), total phenols (21.45 ± 1.54 mg/ml and 26.50 ± 1.22 mg/ml) for aqueous and ethanol stem bark extracts respectively. The extracts scavenged DPPH radical, reduced Fe3+ and inhibited lipid peroxidation. Doxorubicin significantly (p<0.05) lowered the levels of SOD, CAT, GR and TAS and significantly (p<0.05) but, increased the level of LPO. Oral treatment with Vitex doniana extracts significantly (p<0.05) increased the activities of CAT, GR, SOD and TAS while LPO was significantly (p<0.05) lowered. Vitex doniana stem bark extracts significantly (p<0.05) improved the biochemical derangements observed in the induced untreated animals in comparable manner to that of Silymarin. Conclusion: The present study provides the scientific rationale for the use of Vitex doniana stem bark in traditional medicine and has a viable antioxidative capacity both in vitro and in vivo.

scholarly journals Mangiferin Attenuates Myocardial Ischemia-Reperfusion Injury via MAPK/Nrf-2/HO-1/NF-κB In Vitro and In Vivo

2019 ◽  
Vol 2019 ◽  
pp. 1-12 ◽  
Author(s):  
Kun Liu ◽  
Fei Wang ◽  
Shuo Wang ◽  
Wei-Nan Li ◽  
Qing Ye
Keyword(s):  
Oxidative Stress ◽  
Coronary Artery ◽  
Myocardial Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
H9c2 Cells ◽  
Myocardial Ischemia Reperfusion Injury ◽  
Myocardial Ischemia Reperfusion

The aim of this study was to investigate the cardioprotective effect of mangiferin (MAF) in vitro and in vivo. Oxidative stress and inflammatory injury were detected in coronary artery ligation in rats and also in hypoxia-reoxygenation- (H/R-) induced H9c2 cells. MAF inhibited myocardial oxidative stress and proinflammatory cytokines in rats with coronary artery occlusion. The ST segment of MAF treatment groups also resumed. Triphenyltetrazolium chloride (TTC) staining and pathological analysis showed that MAF could significantly reduce myocardial injury. In vitro data showed that MAF could improve hypoxia/reoxygenation- (H/R-) induced H9c2 cell activity. In addition, MAF could significantly reduce oxidative stress and inflammatory pathway protein expression in H/R-induced H9c2 cells. This study has clarified the protective effects of MAF on myocardial injury and also confirmed that oxidative stress and inflammation were involved in the myocardial ischemia-reperfusion injury (I/R) model.

Vinpocetine protects liver against ischemia–reperfusion injury

2013 ◽  
Vol 91 (12) ◽  
pp. 1064-1070 ◽  
Author(s):  
Hala Fahmy Zaki ◽  
Rania Mohsen Abdelsalam
Keyword(s):  
Oxidative Stress ◽  
Inflammatory Cytokines ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Liver Lipid ◽  
Cerebrovascular Disorders ◽  
Cellular Damage ◽  
Dependent Manner ◽  
Oxidative Stress Biomarkers ◽  
Serum Transaminases

Hepatic ischemia–reperfusion (IR) injury is a clinical problem that leads to cellular damage and organ dysfunction mediated mainly via production of reactive oxygen species and inflammatory cytokines. Vinpocetine has long been used in cerebrovascular disorders. This study aimed to explore the protective effect of vinpocetine in IR injury to the liver. Ischemia was induced in rats by clamping the common hepatic artery and portal vein for 30 min followed by 30 min of reperfusion. Serum transaminases and liver lactate dehydrogenase (LDH) activities, liver inflammatory cytokines, oxidative stress biomarkers, and liver histopathology were assessed. IR resulted in marked histopathology changes in liver tissues coupled with elevations in serum transaminases and liver LDH activities. IR also increased the production of liver lipid peroxides, nitric oxide, and inflammatory cytokines interleukin-1β and interleukin-6, in parallel with a reduction in reduced glutathione and interleukin-10 in the liver. Pretreatment with vinpocetine protected against liver IR-induced injury, in a dose-dependent manner, as evidenced by the attenuation of oxidative stress as well as inflammatory and liver injury biomarkers. The effects of vinpocetine were comparable with that of curcumin, a natural antioxidant, and could be attributed to its antioxidant and anti-inflammatory properties.

scholarly journals An Antioxidant Phytotherapy to Rescue Neuronal Oxidative Stress

2011 ◽  
Vol 2011 ◽  
pp. 1-7 ◽  
Author(s):  
Zhihong Lin ◽  
Danni Zhu ◽  
Yongqing Yan ◽  
Boyang Yu ◽  
Qiujuan Wang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Aqueous Extract ◽  
Ischemia Reperfusion ◽  
Brain Infarction ◽  
Reaction System ◽  
Artery Occlusion ◽  
Dependent Manner ◽  
Endogenous Antioxidant

Oxidative stress is involved in the pathogenesis of ischemic neuronal injury. A Chinese herbal formula composed ofPoria cocos(Chinese name:Fu Ling),Atractylodes macrocephala(Chinese name:Bai Zhu) andAngelica sinensis(Chinese names:Danggui, Dong quai, Donggui; Korean name:Danggwi) (FBD), has been proved to be beneficial in the treatment of cerebral ischemia/reperfusion (I/R).This study was carried out to evaluate the protective effect of FBD against neuronal oxidative stressin vivoandin vitro. Rat I/R were established by middle cerebral artery occlusion (MCAO) for 1 h, followed by 24 h reperfusion. MCAO led to significant depletion in superoxide dismutase and glutathione and rise in lipid peroxidation (LPO) and nitric oxide in brain. The neurological deficit and brain infarction were also significantly elevated by MCAO as compared with sham-operated group. All the brain oxidative stress and damage were significantly attenuated by 7 days pretreatment with the aqueous extract of FBD (250 mg kg−1, p.o.). Moreover, cerebrospinal fluid sampled from FBD-pretreated rats protected PC12 cells against oxidative insult induced by 0.2 mM hydrogen peroxide, in a concentration and time-dependent manner (IC5010.6%, ET501.2 h). However, aqueous extract of FBD just slightly scavenged superoxide anion radical generated in xanthine–xanthine oxidase system (IC502.4 mg ml−1) and hydroxyl radical generated in Fenton reaction system (IC503.6 mg ml−1). In conclusion, FBD was a distinct antioxidant phytotherapy to rescue neuronal oxidative stress, through blocking LPO, restoring endogenous antioxidant system, but not scavenging free radicals.

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