scholarly journals NF-κB and FosB mediate inflammation and oxidative stress in the blast lung injury of rats exposed to shock waves

2021 ◽  
Author(s):  
Hong Wang ◽  
Wenjuan Zhang ◽  
Jinren Liu ◽  
Junhong Gao ◽  
Le Fang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Lung Injury ◽  
Shock Waves ◽  
Time Dependent ◽  
Inflammatory Factors ◽  
Control Group ◽  
Dependent Manner ◽  
Total Antioxidant ◽  
Blast Lung Injury ◽  
And Oxidative Stress

Abstract Blast lung injury (BLI) is the major cause of death in explosion-derived shock waves; however, the mechanisms of BLI are not well understood. To identify the time-dependent manner of BLI, a model of lung injury of rats induced by shock waves was established by a fuel air explosive. The model was evaluated by hematoxylin and eosin staining and pathological score. The inflammation and oxidative stress of lung injury were also investigated. The pathological scores of rats’ lung injury at 2 h, 24 h, 3 days, and 7 days post-blast were 9.75±2.96, 13.00±1.85, 8.50±1.51, and 4.00±1.41, respectively, which were significantly increased compared with those in the control group (1.13±0.64; P<0.05). The respiratory frequency and pause were increased significantly, while minute expiratory volume, inspiratory time, and inspiratory peak flow rate were decreased in a time-dependent manner at 2 and 24 h post-blast compared with those in the control group. In addition, the expressions of inflammatory factors such as interleukin (IL)-6, IL-8, FosB, and NF-κB were increased significantly at 2 h and peaked at 24 h, which gradually decreased after 3 days and returned to normal in 2 weeks. The levels of total antioxidant capacity, total superoxide dismutase, and glutathione peroxidase were significantly decreased 24 h after the shock wave blast. Conversely, the malondialdehyde level reached the peak at 24 h. These results indicated that inflammatory and oxidative stress induced by shock waves changed significantly in a time-dependent manner, which may be the important factors and novel therapeutic targets for the treatment of BLI.

scholarly journals TIME COURSE STUDY OF COMBINED N-ACETYL-P-AMINOPHENOL AND DICLOPHENAC INDUCED-HEPATOTOXICITY AND OXIDATIVE STRESS IN WISTAR RATS

2021 ◽  
Vol 46 (2) ◽  
Author(s):  
O. A Dosumu ◽  
D. I. Akinloye ◽  
O. B. Onunkwor ◽  
F. C. Thomas ◽  
R. A. Adeyemo
Keyword(s):  
Oxidative Stress ◽  
Liver Damage ◽  
Wistar Rats ◽  
Time Course ◽  
Time Dependent ◽  
Control Group ◽  
Gamma Glutamyl Transferase ◽  
Dependent Manner ◽  
Glutamyl Transferase ◽  
And Oxidative Stress

The abuse of combined acetaminophen or N-acetyl-p-aminophenol (APAP) and diclofenac (DIC) due to their analgesics, anti-inflammatory and antipyretic properties is a predominant cause of hepatotoxicity and oxidative stress. This study investigated the time-course effects of APAP, DIC and their combination on biomarkers of hepatic function and oxidative stress in rats. Forty male Wistar rats were randomly divided into four groups of 10 animals each as follows; control (distilled water), APAP only, DIC only and APAP + DIC for 4 weeks. Indices of liver damage (serum ALT, alanine aminotransferase; AST, aspartate aminotransferase; ALP, alkaline phosphatase; GGT, gamma-glutamyl transferase and bilirubin) were measured. Oxidative stress biomarkers (MDA, malondialdehyde; NO, nitric oxide; CAT, Catalase activity; SOD, superoxide dismutase activity; GSH content, reduced glutathione), GR, glutathione reductase, and GST, glutathione-S-transferase) were also determined using spectrophotometric methods. Statistical analysis was done using one-way ANOVA with p < 0.05 considered significant. Acetaminophen and diclofenac caused marked liver damage as noted by time-dependent significant (p < 0.05) increased activities of serum ALT, AST, ALP, GGT, and bilirubin levels as well as significant (p < 0.05) increase in hepatic MDA and NO levels as compared to the control group. Hepatic GSH content, SOD, CAT, GPx, GST and GR activities were decreased significantly (p < 0.05) in all acetaminophen and diclofenac-treated groups compared to normal control in a time-dependent manner. These findings suggest that prolonged administration of diclofenac, acetaminophen or their combination may induce hepatotoxicity, oxidative stress and alteration of hepatic antioxidant status in a time-dependent manner.

The Association between Oxidative Stress and Cardiac Functions in Infants Born to Preeclamptic Mothers

2018 ◽  
Vol 36 (11) ◽  
pp. 1205-1210
Author(s):  
Didem Arman ◽  
Secil Ercin ◽  
Sevilay Topcuoğlu ◽  
Ayşem Kaya ◽  
Taner Yavuz ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Premature Infants ◽  
Stress Index ◽  
Control Group ◽  
Cardiac Functions ◽  
Total Antioxidant ◽  
Echocardiographic Parameters ◽  
Oxidant Status ◽  
The Relationship ◽  
And Oxidative Stress

Objective The present study aimed to assess the global oxidant and antioxidant status in infants born to preeclamptic mothers and their correlation with cardiac functions. Study Design We compared 40 infants born to preeclamptic mothers with 40 premature infants born to normotensive mothers. We assessed the relationship between echocardiographic measurements and total antioxidant capacity (TAC) and total oxidant status (TOS) values. Results In the study group, TAC, TOS, and oxidative stress index (OSI) levels were significantly higher in the cord blood (p = 0.03, 0.04, and 0.039, respectively) than in the control group. We did not observe any correlation between echocardiographic measurements and TAC, TOS, and OSI levels in infants born to preeclamptic mothers. Conclusion Compared with the control group, despite higher TAC levels in infants born to preeclamptic mothers, concurrent elevated OSI levels reveal that the oxidant–antioxidant balance is disturbed in favor of oxidants. Furthermore, the findings of this study suggest that echocardiographic parameters are unaffected by the oxidant status.

scholarly journals Effects of Safranal on Tissue Oxidative Stress in Sub-Chronic Thinner-Addicted Rats

2020 ◽  
Vol 71 (1) ◽  
pp. 1997
Author(s):  
M. DÜZ ◽  
A. F. FIDAN
Keyword(s):  
Oxidative Stress ◽  
Nitric Oxide ◽  
Protective Effect ◽  
Total Antioxidant Capacity ◽  
Reduced Glutathione ◽  
Control Group ◽  
Albino Rats ◽  
Total Antioxidant ◽  
Wistar Albino Rats ◽  
And Oxidative Stress

The present study was carried out to determine the effects of sub-chronic thinner addiction on the oxidant-antioxidant balance and oxidative stress on certain tissues and the possible protective effect of safranal against thinner toxication in rats. Adult male Wistar albino rats were randomly divided into four groups of 10 animals each as follows: control (C), safranal (S), thinner (T) and thinner+safranal (T+S). The control group received 1cc saline by gastric gavage. Safranal was administered to S and T+S groups by using gastric gavage at a dose of 100 mg/kg/day and volume of 0.1 mL/kg/day. Thinner inhalation was applied to T and T+S groups in a container with NaOH tablets twice a day. Levels of malondialdehyde (MDA), reduced glutathione (GSH), nitric oxide (NOx) metabolites, total antioxidant capacity (TAS) and total oxidant capacity (TOS) were determined in liver, lung, brain, kidney and testis tissues of the rats. In the T+S group, it was observed that the MDA levels significantly decreased in all tissues, except the kidney, in comparison to the thinner inhalation group (p = 0.000). When the NOx levels of the T+S group were compared with the levels of the T group, it was concluded that there existed a statistically significant decrease in the NOx levels in alltissues (p = 0.000). In T+S group, it was observed that safranal either eliminated or mitigated oxidative stress that developed in tissues through decreasing MDA and TOS levels and increasing GSH and TAS levels and caused significant decreases in NOX levels in all tissues. As a result, it was determined that safranal, although not uniform for all tissue types, had a protective potential against the damaging effects of oxidative stress caused by sub-chronic thinner inhalation.

Salivary Antioxidant and Oxidative Stress Marker Levels in HIV-Positive Individuals

2019 ◽  
Vol 22 (1) ◽  
pp. 59-64
Author(s):  
Samaneh Vaziri Amjad ◽  
Poorandokht Davoodi ◽  
Mohammad Taghi Goodarzi ◽  
Hamidreza Abdolsamadi ◽  
Jalal Poorolajal ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Antioxidant Defense ◽  
Antioxidant Defense System ◽  
Oxidative Stress Marker ◽  
Hiv Positive ◽  
Control Group ◽  
Defense System ◽  
Positive Group ◽  
Total Antioxidant ◽  
And Oxidative Stress

Background:HIV infections are a worldwide health problem. HIV infection reduces CD4+ cell counts. Oxidative stress might play an important role in the stimulation of virus replication and immunodeficiency. Saliva might be the first line of defense against oxidative stress.Objective:The aim of this study was to evaluate the oxidative stress marker and antioxidant levels of saliva in HIV-infected patients by measuring total antioxidant capacity and malondialdehyde level.Methods:A total of 49 HIV-positive patients and 49 healthy HIV-negative individuals were randomly selected. All the patients were clinically examined. Five mL of unstimulated whole saliva was collected and evaluated by spectrophotometric assay. Data were analyzed with STATA 11.Results:Mean ages of the case and control groups were 28 and 33 years, respectively. Salivary malondialdehyde levels were significantly higher in the HIV-positive group (3.68±2.26) compared to the healthy control group (2.79±1.91). Levels of salivary total antioxidant capacity were significantly lower in the HIV-positive group (0.20± 0.09) compared to the control group (0.27±0.10).Conclusion:The antioxidant defense system in HIV-positive individuals was low and oxidative stress was high in this population. Saliva might be used as a diagnostic tool for antioxidant changes in HIV-positive patients in the future. There were changes in salivary antioxidant defense system and oxidative stress in HIV-positive individuals. Antioxidant supplements might help local salivary and general health statuses.

scholarly journals Inhibition of ERRα Aggravates Sepsis-Induced Acute Lung Injury in Rats via Provoking Inflammation and Oxidative Stress

2020 ◽  
Vol 2020 ◽  
pp. 1-9 ◽  
Author(s):  
Wenfang Xia ◽  
Zhou Pan ◽  
Huanming Zhang ◽  
Qingshan Zhou ◽  
Yu Liu
Keyword(s):  
Oxidative Stress ◽  
Acute Lung Injury ◽  
Lung Injury ◽  
Cecal Ligation ◽  
Endothelial Permeability ◽  
Inflammatory Factors ◽  
Inflammatory Factor ◽  
Junction Protein ◽  
And Oxidative Stress

Inflammation and oxidative stress are critical pathologies that contribute to sepsis-induced acute lung injury (ALI). This study investigated the regulatory role of estrogen-related receptor alpha (ERRα) in an experimental model of sepsis-induced ALI. In vivo, a cecal ligation and puncture- (CLP-) induced ALI model was established in anesthetized rats. Animals were then randomly assigned to receive an intraperitoneal injection of vehicle or ERRα inverse agonist (XCT-790, 2.5 mg/kg). Administration of XCT-790 significantly aggravated a sepsis-induced increase in pathological damage of lung tissues, lung endothelial permeability, myeloperoxidase (MPO) activity in lung tissues, production of serum inflammatory factors, and inflammatory cell accumulation in bronchoalveolar lavage fluid. In addition, XCT-790 treatment exacerbated a CLP-induced decrease in lung superoxide dismutase and an increase in lung malondialdehyde levels. In vitro, the exposure of rat pulmonary microvascular endothelial cells (PMVECs) to lipopolysaccharide (LPS) resulted in increased endothelial permeability and reduced expression of tight junction protein ZO-1, Occludin, JAM-A, and adherens junction protein VE-cadherin, which were further deteriorated by knockdown of ERRα. In addition, LPS-triggered inflammatory factor production and increase in the expression of phosphorylated IκBα and NF-κB p65 were also exacerbated by silencing ERRα gene. Meanwhile, knockdown of ERRα dramatically promoted LPS-activated mitochondrial reactive oxygen species production and LPS-induced downregulation of Sirt3 protein levels in rat PMVECs. Taken together, our present study provides evidences that ERRα functions as a novel negative modulator of sepsis-induced ALI in rats. The underlying mechanisms responsible for ERRα-elicited effects are largely dependent on the regulation of inflammatory response and oxidative stress.

scholarly journals Consumption of Hydrogen Water Reduces Paraquat-Induced Acute Lung Injury in Rats

2011 ◽  
Vol 2011 ◽  
pp. 1-7 ◽  
Author(s):  
Shulin Liu ◽  
Kan Liu ◽  
Qiang Sun ◽  
Wenwu Liu ◽  
Weigang Xu ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Acute Lung Injury ◽  
Lung Injury ◽  
Molecular Hydrogen ◽  
Pure Water ◽  
Control Group ◽  
Sprague Dawley ◽  
Hydrogen Water ◽  
Sd Rats ◽  
And Oxidative Stress

Exposure to paraquat leads to acute lung injury and oxidative stress is widely accepted as a contributor to paraquat-induced acute lung injury. Recent studies have reported that consumption of water with dissolved molecular hydrogen to a saturated level (hydrogen water) prevents oxidative stress-induced diseases. Here, we investigated whether consumption of saturated hydrogen saline protects rats against paraquat-induced acute lung injury. Adult male Sprague-Dawley (SD) rats were randomly divided into four groups: Control group; hydrogen water-only group (HW group); paraquat-only group (PQ group); paraquat and hydrogen water group (PQ  +  HW group). The rats in control group and HW group drank pure water or hydrogen water; the rats in PQ group and PQ  +  HW group were intraperitonealy injected with paraquat (35 mg/kg) and then provided pure water or hydrogen water. Both biochemical and histological lung alterations were measured. The results showed that hydrogen water ameliorated these alterations, demonstrating that hydrogen water alleviated paraquat-induced acute lung injury possibly by inhibition of oxidative damage.

scholarly journals Mucin1 relieves acute lung injury by inhibiting inflammation and oxidative stress

2021 ◽  
Vol 65 (4) ◽  
Author(s):  
Chunlin Ye ◽  
Bin Xu ◽  
Jie Yang ◽  
Yunkun Liu ◽  
Zhikai Zeng ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Acute Lung Injury ◽  
Lung Injury ◽  
Respiratory Distress ◽  
Signaling Pathway ◽  
Lung Tissue ◽  
Inflammatory Factors ◽  
Mouse Lung ◽  
Muc1 Gene ◽  
And Oxidative Stress

Acute lung injury/acute respiratory distress syndrome (ALI/ARDS) is a kind of diffuse inflammatory injury caused by various factors, characterized by respiratory distress and progressive hypoxemia. It is a common clinical critical illness. The aim of this study was to investigate the effect and mechanism of the Mucin1 (MUC1) gene and its recombinant protein on lipopolysaccharide (LPS)-induced ALI/ARDS. We cultured human alveolar epithelial cell line (BEAS-2B) and used MUC1 overexpression lentivirus to detect the effect of MUC1 gene on BEAS-2B cells. In addition, we used LPS to induce ALI/ARDS in C57/BL6 mice and use hematoxylin and eosin (H&E) staining to verify the effect of their modeling. Recombinant MUC1 protein was injected subcutaneously into mice. We examined the effect of MUC1 on ALI/ARDS in mice by detecting the expression of inflammatory factors and oxidative stress molecules in mouse lung tissue, bronchoalveolar lavage fluid (BALF) and serum. Overexpression of MUC1 effectively ameliorated LPS-induced damage to BEAS-2B cells. Results of H&E staining indicate that LPS successfully induced ALI/ARDS in mice and MUC1 attenuated lung injury. MUC1 also reduced the expression of inflammatory factors (IL-1β, TNF-α, IL-6 and IL-8) and oxidative stress levels in mice. In addition, LPS results in an increase in the activity of the TLR4/NF-κB signaling pathway in mice, whereas MUC1 decreased the expression of the TLR4/NF-κB signaling pathway. MUC1 inhibited the activity of TLR4/NF-κB signaling pathway and reduced the level of inflammation and oxidative stress in lung tissue of ALI mice.

scholarly journals BISPHENOL A DOSE- AND TIME-DEPENDENTLY INDUCES OXIDATIVE STRESS IN RAT LIVER MITOCHONDRIA EX VIVO

2018 ◽  
Vol 11 (9) ◽  
pp. 98 ◽  
Author(s):  
Mousumi Dutta ◽  
Goutam Paul
Keyword(s):  
Oxidative Stress ◽  
Bisphenol A ◽  
Rat Liver ◽  
Ex Vivo ◽  
Liver Mitochondria ◽  
Time Dependent ◽  
Incubation Mixture ◽  
Rat Liver Mitochondria ◽  
Control Group ◽  
Dependent Manner

Objective: The probable toxic effects of bisphenol A (BPA) on different physiological functions have been reported in animal models. The role of BPA in mitochondrial oxidative stress has not been reported till date. The present study is aimed to elucidate dose- and time-dependent oxidative stress generation by BPA, respectively, in rat liver mitochondria in ex vivo model. Methods: The incubation mixture of BPA-treated groups containing mitochondria, 50 mM potassium phosphate buffer (pH 7.4), and different concentrations of BPA (20–160 μM/ml) (dissolved in 12% DMSO) in a final volume of 1.0 ml was incubated at 37°C in incubator for different time durations (30 min–2 h). Whereas, the incubation mixture of control group contained DMSO (12%), mitochondria and 50 mM potassium phosphatebuffer (pH 7.4).’ will be replaced by ‘Whereas, the incubation mixture of control group contained the same constituents except BPA. Result: We have observed significant decrease in mitochondrial intactness incubated with BPA in dose- and time-dependent manner under bright field and confocal microscopic study compared to control. Further, we have observed a decrease in mitochondrial reduced glutathione (GSH) content and increase in lipid peroxidation and protein carbonylation levels in dose- and time-dependent manner in BPA-exposed mitochondria. We have found a significant increase in the activity of Mn-superoxide dismutase and decrease in the activities of GSH peroxidase, GSH reductase, pyruvate dehydrogenase, and other three enzymes of Kreb’s cycle dose and time dependently in BPA-exposed mitochondria. The results indicate that exposure to BPA leads to decrease in intactness of mitochondria and increase in oxidative stress in mitochondria isolated from rat liver in a dose- and time-dependent manner. Conclusion: It can be concluded that the incubation of mitochondria isolated from rat liver with BPA, caused oxidative stress-mediated damages in mitochondria in both dose- and time-dependent manners.

scholarly journals Human Urinary Kallidinogenase Reduces Lipopolysaccharide-Induced Neuroinflammation and Oxidative Stress in BV-2 Cells

2019 ◽  
Vol 2019 ◽  
pp. 1-6 ◽  
Author(s):  
Zhongyan Zhao ◽  
Zhiyu Xu ◽  
Tao Liu ◽  
Shixiong Huang ◽  
Huai Huang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Neurological Disorders ◽  
Interleukin 1 ◽  
Control Group ◽  
Tissue Kallikrein ◽  
Dependent Manner ◽  
Socioeconomic Burden ◽  
Dose Dependent ◽  
And Oxidative Stress ◽  
Necrosis Factor

Migraine is one of the most common neurological disorders which poses significant socioeconomic burden worldwide. Neuroinflammation and oxidative stress both play important roles in the pathogenesis of migraine. Human urinary kallidinogenase (UK) is a tissue kallikrein derived from human urine. Increasing evidence suggests that UK may protect against ischemic stroke, but UK’s treatment potential against migraine remains to be explored. Immortal BV-2 murine microglial cells were treated with UK (125 nM, 250 nM, and 500 nM) and then given lipopolysaccharides (LPS, 1000 ng/mL). Cell viability of BV-2 cells was tested by the CCK-8 assay. Expressions of tumor necrosis factor-α (TNFα), prostaglandin E2 (PGE2), interleukin-6 (IL-6), and interleukin-1β (IL-1β) were examined with the ELISA method and western blot. Intracellular reactive oxygen species (ROS) and malondialdehyde (MDA) were measured to determine oxidative stress. Our results showed that LPS administration increased the levels of proinflammatory cytokines (TNFα, PGE2, IL-6, and IL-1β) and oxidative stress (ROS and MDA) when compared with the control group and decreased significantly upon introduction with UK. Taken together, UK treatment reduced LPS-induced neuroinflammation and oxidative stress in a dose-dependent manner, which might be a potential treatment of migraine.

scholarly journals Evaluation of Uric Acid, Total Antioxidant and Lipid Peroxidation Parameters in Serum and Saliva of Patients with Oral Lichen Planus

2016 ◽  
Vol 8 (12) ◽  
pp. 225 ◽  
Author(s):  
Atena Shiva ◽  
Shahin Arab
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Lichen Planus ◽  
Oral Lichen Planus ◽  
Control Group ◽  
Healthy Controls ◽  
Total Antioxidant ◽  
Healthy Control ◽  
Oral Lichen ◽  
And Oxidative Stress

<p><strong>BACKGROUND</strong><strong>: </strong>Oral lichen planus (OLP) is a chronic and inflammation mucosal disease. Reactive Oxygen Species (ROS) and oxidative stress damage might be the cause. Malondialdehyd (MDA), one parameter of lipid peroxidation is appropriate for DNA damage in OLP disease.</p><p><strong>OBJECTIVE</strong><strong>: </strong>To evaluate antioxidants and oxidative stress parameters in patients with oral lichen planus (OLP) diseases and healthy control group with compare on serum and salivary samples.</p><p><strong>MATERIAL </strong><strong>&amp;</strong><strong> METHODS: </strong>The research population included 22 patients with OLP which recently diagnosed and 22 healthy controls matched for periodontal status. Total antioxidant activity (TAA), Malondialdehyde (MDA) or lipid peroxidation product and uric acid (UA) were evaluated in both serum and saliva. The t-tests were used for differences between the two groups in normal distributed variables and also Spearman’s rho correlation coefficient for assessing association between serum and salivary fluids.</p><p><strong>RESULTS</strong><strong>: </strong>TAA levels in OLP patients showed significant result and lower than healthy control group (p=0.39). Also, results in the saliva MDA concentration, was significantly higher in OLP patients than controls. In correlation test, inverse and significant correlation was observed between the MDA and UA values(r=0. 682, P=0.0001) and a significant correlation was found between serum TAA and UA values.</p><p><strong>CONCLUSION</strong><strong>: </strong>This study showed that OLP groups have higher cellular lipid peroxidation in compare to healthy controls and low level of TAA than controls. Patients with OLP are believed to be more at risk of antioxidant-oxidative stress imbalance.</p>

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