scholarly journals Choline and Cystine Deficient Diets in Animal Models with Hepatocellular Injury: Evaluation of Oxidative Stress and Expression of RAGE, TNF-α, and IL-1β

2015 ◽  
Vol 2015 ◽  
pp. 1-11 ◽  
Author(s):  
Juliana Célia F. Santos ◽  
Orlando R. P. de Araújo ◽  
Iara B. Valentim ◽  
Kívia Queiroz de Andrade ◽  
Fabiana Andréa Moura ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Animal Models ◽  
Hepatic Steatosis ◽  
Hepatic Injury ◽  
Young Male ◽  
Thiobarbituric Acid ◽  
Hepatocellular Injury ◽  
Oxidative Stress Biomarkers ◽  
Tnf Α ◽  
Male Wistar Rats

This study aims to evaluate the effects of diets deficient in choline and/or cystine on hepatocellular injury in animal models (young male Wistar rats, aged 21 days), by monitoring some of the oxidative stress biomarkers and the expression of RAGE, TNF-α, and IL-1β. The animals were divided into 6 groups (n=10) and submitted to different diets over 30 days: AIN-93 diet (standard, St), AIN-93 choline deficient (CD) diet and AIN-93 choline and cystine deficient (CCD) diet, in the pellet (pl) and powder (pw) diet forms. Independently of the diet form, AIN-93 diet already led to hepatic steatosis and CD/CCD diets provoked hepatic damage. The increase of lipid peroxidation, represented by the evaluation of thiobarbituric acid reactive species, associated with the decrease of levels of antioxidant enzymes, were the parameters with higher significance toward redox profile in this model of hepatic injury. Regarding inflammation, in relation to TNF-α, higher levels were evidenced inCD(pl), while, for IL-1β, no significant alteration was detected. RAGE expression was practically the same in all groups, with exception ofCCD(pw)versusCCD(pl). These results together confirm that AIN-93 causes hepatic steatosis and choline and/or cysteine deficiencies produce important hepatic injury associated with oxidative stress and inflammatory profiles.

scholarly journals Importance of the Use of Oxidative Stress Biomarkers and Inflammatory Profile in Aqueous and Vitreous Humor in Diabetic Retinopathy

Antioxidants ◽  
2020 ◽  
Vol 9 (9) ◽  
pp. 891 ◽  
Author(s):  
Ana Karen López-Contreras ◽  
María Guadalupe Martínez-Ruiz ◽  
Cecilia Olvera-Montaño ◽  
Ricardo Raúl Robles-Rivera ◽  
Diana Esperanza Arévalo-Simental ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Diabetic Retinopathy ◽  
High Concentration ◽  
Oxidative Stress Biomarkers ◽  
Retinal Microvasculature ◽  
Tnf Α ◽  
Long Time ◽  
Markers Of Oxidative Stress ◽  
Cyt C ◽  
Inflammatory Profile

Diabetic retinopathy is one of the leading causes of visual impairment and morbidity worldwide, being the number one cause of blindness in people between 27 and 75 years old. It is estimated that ~191 million people will be diagnosed with this microvascular complication by 2030. Its pathogenesis is due to alterations in the retinal microvasculature as a result of a high concentration of glucose in the blood for a long time which generates numerous molecular changes like oxidative stress. Therefore, this narrative review aims to approach various biomarkers associated with the development of diabetic retinopathy. Focusing on the molecules showing promise as detection tools, among them we consider markers of oxidative stress (TAC, LPO, MDA, 4-HNE, SOD, GPx, and catalase), inflammation (IL-6, IL-1ß, IL-8, IL-10, IL-17A, TNF-α, and MMPs), apoptosis (NF-kB, cyt-c, and caspases), and recently those that have to do with epigenetic modifications, their measurement in different biological matrices obtained from the eye, including importance, obtaining process, handling, and storage of these matrices in order to have the ability to detect the disease in its early stages.

scholarly journals Protective Role of Probiotic Supplements in Hepatic Steatosis: A Rat Model Study

2020 ◽  
Vol 2020 ◽  
pp. 1-15 ◽  
Author(s):  
Aein Azarang ◽  
Omid Farshad ◽  
Mohammad Mehdi Ommati ◽  
Akram Jamshidzadeh ◽  
Reza Heidari ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Hepatic Steatosis ◽  
Bacillus Coagulans ◽  
Male Rats ◽  
Health Priorities ◽  
Oxidative Stress Markers ◽  
Oxidative Stress Biomarkers ◽  
Nonalcoholic Fatty Liver ◽  
Stress Markers ◽  
And Oxidative Stress

Background. Treating nonalcoholic fatty liver disease (NAFLD) is considered one of the public health priorities in the past decade. So far, probiotics have represented promising results in controlling the signs and symptoms of NAFLD. However, attempts to find the ideal probiotic strain are still ongoing. The present study is designed to find the best strain amongst suitable probiotic strains according to their ability to ameliorate histopathological and oxidative stress biomarkers in hepatic steatosis-induced rats. Methods. Initially, four probiotics species, including Lactobacillus (L.) acidophilus, L. casei, L. reuteri, and Bacillus coagulans, were cultured and prepared as a lyophilized powder for animals. The experiment lasted for fifty days. Initially, hepatic steatosis was induced by excessive ingestion of D-fructose in rats for eight weeks, followed by eight weeks of administering probiotics and D-fructose concurrently. Forty-two six-week-old male rats were alienated to different groups and were supplemented with different probiotics ( 1 ∗ 10 9   CFU in 500 mL drinking water). After eight weeks, blood and liver samples were taken for further evaluation, and plasma and oxidative stress markers corresponding to liver injuries were examined. Results. Administration of probiotics over eight weeks reversed hepatic and blood triglyceride concentration and blood glucose levels. Also, probiotics significantly suppressed markers of oxidative stress in the liver tissue. Conclusions. Although some of the single probiotic formulations were able to mitigate oxidative stress markers, mixtures of probiotics significantly ameliorated more symptoms in the NAFLD animals. This enhanced effect might be due to probiotics’ cumulative potential to maintain oxidative stress and deliver improved lipid profiles, liver function markers, and inflammatory markers.

scholarly journals Opposing Effects of Oxygen Regulation on Kallistatin Expression: Kallistatin as a Novel Mediator of Oxygen-Induced HIF-1-eNOS-NO Pathway

2017 ◽  
Vol 2017 ◽  
pp. 1-8 ◽  
Author(s):  
Julie Chao ◽  
Youming Guo ◽  
Pengfei Li ◽  
Lee Chao
Keyword(s):  
Oxidative Stress ◽  
Endothelial Cells ◽  
Animal Models ◽  
Hypoxia Inducible Factor ◽  
Thiobarbituric Acid ◽  
Organ Injury ◽  
Thiobarbituric Acid Reactive Substance ◽  
Bacterial Killing ◽  
Antioxidant Genes ◽  
Pkc Activation

Oxidative stress has both detrimental and beneficial effects. Kallistatin, a key component of circulation, protects against vascular and organ injury. Serum kallistatin levels are reduced in patients and animal models with hypertension, diabetes, obesity, and cancer. Reduction of kallistatin levels is inversely associated with elevated thiobarbituric acid-reactive substance. Kallistatin therapy attenuates oxidative stress and increases endothelial nitric oxide synthase (eNOS) and NO levels in animal models. However, kallistatin administration increases reactive oxygen species formation in immune cells and bacterial killing activity in septic mice. High oxygen inhibits kallistatin expression via activating the JNK-FOXO1 pathway in endothelial cells. Conversely, mild oxygen/hyperoxia stimulates kallistatin, eNOS, and hypoxia-inducible factor-1 (HIF-1) expression in endothelial cells and in the kidney of normal mice. Likewise, kallistatin stimulates eNOS and HIF-1, and kallistatin antisense RNA abolishes oxygen-induced eNOS and HIF-1 expression, indicating a role of kallistatin in mediating mild oxygen’s stimulation on antioxidant genes. Protein kinase C (PKC) activation mediates HIF-1-induced eNOS synthesis in response to hyperoxia/exercise; thus, mild oxygen through PKC activation stimulates kallistatin-mediated HIF-1 and eNOS synthesis. In summary, oxidative stress induces down- or upregulation of kallistatin expression, depending on oxygen concentration, and kallistatin plays a novel role in mediating oxygen/exercise-induced HIF-1-eNOS-NO pathway.

scholarly journals Effect of Antioxidant Treatment on Fibrogenesis in Rats with Carbon Tetrachloride-Induced Cirrhosis

2012 ◽  
Vol 2012 ◽  
pp. 1-7 ◽  
Author(s):  
Silvia Bona ◽  
Lidiane Isabel Filippin ◽  
Fábio Cangeri Di Naso ◽  
Cintia de David ◽  
Bruna Valiatti ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Wistar Rats ◽  
Reduced Glutathione ◽  
Thiobarbituric Acid ◽  
Matrix Metalloproteinase 2 ◽  
Glutathione Disulfide ◽  
Antioxidant Treatment ◽  
P450 Enzyme ◽  
Male Wistar Rats ◽  
Increased Activity

Aim. This study aimed to assess the antioxidant activity of quercetin (Q) in an experimental model of cirrhosis induced by CCl4 inhalation. Materials and Methods. We used 25 male Wistar rats (250 g) that were divided into 3 groups: control (CO), CCl4, and CCl4+Q. The rats were subjected to CCl4 inhalation (2x/week) for 16 weeks, and they received phenobarbital in their drinking water at a dose of 0.3 g/dL as a P450 enzyme inducer. Q (50 mg/Kg) was initiated intraperitoneally at 10 weeks of inhalation and lasted until the end of the experiment. Statistical analysis was by ANOVA Student Newman-Keuls (mean±SEM), and differences were considered statistically significant when P<0.05. Results. After treatment with quercetin, we observed an improvement in liver complications, decreased fibrosis, as analyzed by picrosirius for the quantification of collagen, and decreased levels of matrix metalloproteinase 2 (MMP-2) compared with the CCl4 group. It also reduced oxidative stress, as confirmed by the decrease of substances reacting to thiobarbituric acid (TBARS), the increased activity of antioxidant enzymes, and the reduced glutathione ratio and glutathione disulfide (GSH/GSSG). Conclusion. We suggest that the use of quercetin might be promising as an antioxidant therapy in liver fibrosis.

scholarly journals Effect of Running Exercise on Oxidative Stress Biomarkers: A Systematic Review

2021 ◽  
Vol 11 ◽  
Author(s):  
Anand Thirupathi ◽  
Ricardo A. Pinho ◽  
Ukadike C. Ugbolue ◽  
Yuhuan He ◽  
Yao Meng ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Oxidative Damage ◽  
Thiobarbituric Acid ◽  
Protein Carbonyl ◽  
Enzymatic Antioxidants ◽  
Oxidative Stress Biomarkers ◽  
Running Exercise ◽  
Exercise Induced ◽  
The Individual ◽  
Meta Analyses

Background: Exercise induced health benefits are limited by the overaccumulation of reactive oxygen species (ROS). ROS and further oxidative stress could potentially induce muscle damage which could result in poor exercise performance. However, predicting ROS induced oxidative stress in response to endurance training has several limitations in terms of selecting biomarkers that are used to measure oxidative stress.Objective: The purpose of this study was to systematically investigate the suitable biomarkers that predict oxidative stress status among runners.Methods: According to the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) statement, a search for relevant articles was carried out on PubMed/Medline, ISI Web of Science, and Google Scholar using related search terms such as oxidative damage, ROS, exercise, physical training, running, marathon, and ultramarathon.Results: Outcomes included (1) running programs like a half-marathon, ultramarathon, and iron-man race, (2) measuring biochemical assessment of oxidative damage markers such as malondialdehyde (MDA), protein carbonyl (PC), total antioxidant capacity (TAC), thiobarbituric acid reactive substances (TBARS), 8-Oxo-2'-deoxyguanosine (8-OH-dG), 4-hydroxynonenal (HNE), and F1-isoprostones, and enzymatic and non-enzymatic antioxidants level.Conclusions: This study concluded that a running exercise does not elicit a response to specific biomarkers of oxidative stress, instead, oxidative damage markers of lipids, proteins, and various enzymatic and non-enzymatic antioxidants are expressed according to the training status of the individual.

scholarly journals Association between Vitamin D Supplements, Oxidative Stress Biomarkers, and Hyperbaric Therapy in Patients with Sudden Sensorineural Hearing Loss

2021 ◽  
Vol 2021 ◽  
pp. 1-10
Author(s):  
Jarosław Paprocki ◽  
Paweł Sutkowy ◽  
Jacek Piechocki ◽  
Alina Woźniak
Keyword(s):  
Oxidative Stress ◽  
Vitamin D ◽  
Hearing Loss ◽  
Sensorineural Hearing Loss ◽  
Thiobarbituric Acid ◽  
Vitamin D Supplementation ◽  
Sudden Sensorineural Hearing Loss ◽  
Sensorineural Hearing ◽  
Oxidative Stress Biomarkers ◽  
Stress Markers

The effect of vitamin D supplementation to patients with sudden sensorineural hearing loss (SSNHL), treated with hyperbaric oxygen (HBO) therapy, on the markers of the oxidant-antioxidant equilibrium was investigated. Patients were divided into two groups: those who did and did not receive vitamin D (cholecalciferol at 4000 IU/24 h). Concentrations of the following compounds, thiobarbituric acid reactive substances (TBARS), malondialdehyde (MDA), conjugated dienes (CD) in plasma and erythrocytes and activities of catalase (CAT), superoxide dismutase (SOD) and glutathione peroxidase (GPx) in erythrocytes, were determined. Haemoglobin (HGB) and haematocrit (HCT) were measured. Blood for analyses was collected from the basilic vein at three time points: before the first HBO procedure, up to 5 min after the first procedure, and after 14 procedures. No statistically significant differences in parameters tested were found between patients who did and did not receive vitamin D. In patients without supplementation, an increase of 53.2% ( P ≤ 0.05 ) in erythrocyte TBARS was observed after the first HBO treatment. In patients receiving vitamin D, a reduction of 27.6% ( P ≤ 0.05 ) was observed in erythrocyte MDA after 14 HBO treatments vs. that after the first treatment. In both groups, a decrease of 33.3% in plasma CD was observed after 14 treatments vs. that after the first treatment ( P ≤ 0.05 and P ≤ 0.01 , respectively). No statistically significant changes were observed in the erythrocyte SOD, GPx, and CAT activities and in HCT. A reduction of HGB concentration of 10.9% ( P ≤ 0.05 ) was demonstrated in nonsupplemented patients after 14 treatments compared with baseline. The results confirm that the effect of HBO therapy on oxidative stress markers is inconclusive and complex. Repeated HBO procedures can induce adaptive changes which protect against disruption of the oxidant-antioxidant equilibrium. It is possible that vitamin D supplementation inhibits the process of lipid peroxidation in erythrocytes.

Preventive effect of curcumin on inflammation, oxidative stress and insulin resistance in high-fat fed obese rats

2016 ◽  
Vol 13 (2) ◽  
Author(s):  
Nachimuthu Maithilikarpagaselvi ◽  
Magadi Gopalakrishna Sridhar ◽  
Rathinam Palamalai Swaminathan ◽  
Ramalingam Sripradha
Keyword(s):  
Oxidative Stress ◽  
Insulin Resistance ◽  
Skeletal Muscle ◽  
Body Weight ◽  
Density Lipoprotein ◽  
High Fat ◽  
Oxidative Stress Parameters ◽  
Tnf Α ◽  
Male Wistar Rats ◽  
Fat Feeding

Abstract: The present study investigated the beneficial effects of curcumin on inflammation, oxidative stress and insulin resistance in high-fat fed male Wistar rats.: Five-month-old male Wistar rats (n=20) were divided into two groups (10 rats in each group). Among the two groups, one group received 30 % high-fat diet (HFD) and another group received 30 % HFD with curcumin (200 mg/kg body weight). Food intake, body weight and biochemical parameters were measured at the beginning and at the end of the study. After 10 weeks, oxidative stress parameters in skeletal muscle and hepatic triacylglycerol (TAG) content were estimated. Histological examinations of the liver samples were performed at the end of the experiment.: High-fat feeding caused increase in body weight, liver and adipose tissue mass. Rats fed with HFD showed increased levels of fasting plasma glucose, insulin, Homeostasis Model Assessment for Insulin resistance (HOMA-IR), total cholesterol (TC), TAG, very low density lipoprotein cholesterol (VLDL-c) and decreased high-density lipoprotein cholesterol (HDL-c). There was also increase in the plasma inflammatory markers [tumor necrosis factor-α (TNF-α), C-reactive protein (CRP)] and skeletal muscle oxidative stress parameters [malondialdehyde (MDA), total oxidant status (TOS)] in these rats. In addition, high-fat feeding increased liver TAG content and caused fat accumulation in the liver. Treatment with curcumin significantly reduced body weight, relative organ weights (liver, adipose tissue), glucose, insulin and HOMA-IR. Curcumin supplementation decreased plasma levels of TC, TAG, VLDL-c, TNF-α and increased HDL-c. Administration of curcumin also reduced MDA, TOS in skeletal muscle, hepatic TAG content and liver fat deposition.: Curcumin supplementation improved HFD-induced dyslipidemia, oxidative stress, inflammation and insulin resistance.

Necroptosis is a key pathogenic event in human and experimental murine models of non-alcoholic steatohepatitis

2015 ◽  
Vol 129 (8) ◽  
pp. 721-739 ◽  
Author(s):  
Marta B. Afonso ◽  
Pedro M. Rodrigues ◽  
Tânia Carvalho ◽  
Marta Caridade ◽  
Paula Borralho ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Hepatic Steatosis ◽  
Murine Models ◽  
Alcoholic Steatohepatitis ◽  
Regulated Necrosis ◽  
Tnf Α ◽  
And Oxidative Stress

Focusing on regulated necrosis in the liver, this study demonstrates that necroptosis contributes to NAFLD pathogenesis in humans and in experimental murine models of hepatic steatosis and NASH. Further, it establishes the involvement of TNF-α and oxidative stress in necroptotic signalling in hepatocytes.

scholarly journals Human placental extract ameliorates methotrexate-induced hepatotoxicity in rats via regulating antioxidative and anti-inflammatory responses

2021 ◽  
Author(s):  
Mamdooh Ghoneum ◽  
Mohamed S. A. El-Gerbed
Keyword(s):  
Oxidative Stress ◽  
Inflammatory Responses ◽  
Biological Effects ◽  
Cellular Damage ◽  
Male Rats ◽  
Antioxidant Enzyme Activities ◽  
Oxidative Stress Biomarkers ◽  
Tnf Α ◽  
Anti Inflammatory ◽  
Liver Tissues

Abstract Purpose Methotrexate (MTX) induces hepatotoxicity, limiting its clinical efficacy as a widely known chemotherapy drug. In the current study, we examined the protective effect of human placenta extract (HPE) against MTX-induced liver damage in rats, as well as its ability to regulate antioxidative and anti-inflammatory liver responses. Methods Male rats were orally administered MTX at a daily dose of 5 mg/kg-body-weight in the presence or absence of HPE (10.08 mg/kg) for 2 weeks. We measured the biological effects of MTX and HPE on the levels of liver enzymes, lipid profile, lipid peroxidation, oxidative stress biomarkers, and cytokines [tumor necrosis factor alpha (TNF-α), interleukin-6 (IL-6), and interleukin-10 (IL-10)]. In addition, histological examination and histopathological scoring of liver tissues were performed. Results MTX-treated rats showed significantly increased (p < 0.001) liver enzyme levels for aspartate aminotransferase (AST), alanine aminotransferase (ALT), alkaline phosphatase (ALP), total bilirubin, total cholesterol, and triglyceride levels. However, HPE supplementation in MTX-treated rats significantly decreased (p < 0.001) these elevated levels. HPE supplementation also significantly reduced the oxidative stress biomarker malondialdehyde (MDA), reversed the reduction in glutathione (GSH), and markedly increased the antioxidant enzyme activities of catalase (CAT) and superoxide dismutase (SOD) in the livers of MTX-treated rats. Furthermore, HPE supplementation significantly decreased the MTX-elevated levels of the pro-inflammatory cytokines TNF-α, IL-6, and IL-10. Histopathological examinations showed that MTX produced severe cellular damage and inflammatory lesions in liver tissues, while treatment with HPE improved hepatic histologic architecture. Conclusion HPE has the ability to ameliorate methotrexate-induced liver injury in rats by mechanisms that include boosting antioxidative responses and down-regulating MDA and pro-inflammatory cytokine production.

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