scholarly journals Toxicity of DON on GPx1-Overexpressed or Knockdown Porcine Splenic Lymphocytes In Vitro and Protective Effects of Sodium Selenite

2019 ◽  
Vol 2019 ◽  
pp. 1-24 ◽  
Author(s):  
Zhihua Ren ◽  
Changhao Chen ◽  
Yu Fan ◽  
Chaoxi Chen ◽  
Hongyi He ◽  
...  
Keyword(s):  
Dna Methylation ◽  
Antioxidant Capacity ◽  
Sodium Selenite ◽  
Animal Feed ◽  
Cell Damage ◽  
The Body ◽  
Dependent Manner ◽  
Protective Effects ◽  
Splenic Lymphocytes ◽  
Apoptosis Rate

Deoxynivalenol (DON) is a common contaminant of grain worldwide and is often detected in the human diet and animal feed. Selenium is an essential trace element in animals. It has many biological functions. The role of selenium in the body is mainly orchestrated by selenoprotein. Glutathione peroxidase (GPx) also exists widely in the body and has attracted much attention due to its high antioxidant capacity. In order to explore the effect of the GPx1 gene on toxicity of DON, in this study, we overexpressed or knockdown GPx1 in porcine splenic lymphocytes, then added different concentrations of DON (0.1025, 0.205, 0.41, and 0.82 μg/mL) and sodium selenite (2 μmol/L) to the culture system. Using various techniques, we detected antioxidant function, free radical content, cell apoptosis, and methylation-related gene expression to explore the effect of GPx1 expression on DON-induced cell damage. We also explored whether selenium can antagonize the toxicity of DON in these two cell models and revealed the protective effect of sodium selenite on DON-induced cell damage in GPx1-overexpressing or knockdown splenic lymphocytes. Finally, our findings revealed the following: (1) GPx1 can regulate the antioxidant capacity, apoptosis rate, and expression of DNA methylation-related genes in pig splenic lymphocytes. (2) Na2SeO3 (2 μmol/L) can regulate the antioxidant capacity, apoptosis rate, and expression of DNA methylation-related genes in pig splenic lymphocytes, and this effect is more significant in GPx1-overexpressing cells than in GPx1-knockdown cells. (3) DON can cause oxidative damage, apoptosis, and methylation injury in GPx1-overexpressing or knockdown pig splenic lymphocytes in a concentration-dependent manner. (4) Na2SeO3 (2 μmol/L) can antagonize the toxic effect of DON on GPx1-overexpressing or knockdown pig splenic lymphocytes. Our findings may have important implications for food/feed safety, human health, and environmental protection.

scholarly journals TAK-875 Mitigates β-Cell Lipotoxicity-Induced Metaflammation Damage through Inhibiting the TLR4-NF-κB Pathway

2019 ◽  
Vol 2019 ◽  
pp. 1-11 ◽  
Author(s):  
Xide Chen ◽  
Yuanli Yan ◽  
Zhiyan Weng ◽  
Chao Chen ◽  
Miaoru Lv ◽  
...  
Keyword(s):  
Islet Cells ◽  
Cell Damage ◽  
The Body ◽  
Inflammatory Factors ◽  
Dependent Manner ◽  
Protective Effects ◽  
Concentration Dependent Manner ◽  
Major Mechanism ◽  
B Subunit

Metabolic inflammatory damage, characterized by Toll-like receptor 4 (TLR4) signaling activation, is a major mechanism underlying lipotoxicity-induced β-cell damage. The present study is aimed at determining whether G protein-coupled receptor 4 (GPR40) agonist can improve β-cell lipotoxicity-induced damage by inhibiting the TLR4-NF-κB pathway. Lipotoxicity, inflammation-damaged β-cells, obese SD, and TLR4KO rat models were used in the study. In vitro, TAK-875 inhibited the lipotoxicity- and LPS-induced β-cell apoptosis in a concentration-dependent manner, improved the insulin secretion, and inhibited the expression of TLR4 and NF-κB subunit P65. Besides, silencing of TLR4 expression enhanced the protective effects of TAK-875, while TLR4 overexpression attenuated this protective effect. Activation of TLR4 or NF-κB attenuated the antagonism of TAK-875 on PA-induced damage. Moreover, the above process of TAK-875 was partially independent of GPR40 expression. TAK-875 reduced the body weight and inflammatory factors, rebalanced the number and distribution of α or β-cells, inhibited the apoptosis of islet cells, and inhibited the expression of TLR4 and NF-κB subunit P65 in obese rats. Further knockout of the rat TLR4 gene delayed the damage induced by the high-fat diet and synergy with the action of TAK-875. These data suggest that GPR40 agonists antagonized the lipotoxicity β-cell damage by inhibiting the TLR4-NF-κB pathway.

scholarly journals Variation in radical antioxidant capacity and the total amount of carotenoids in razor clams, Ensis marginatus (Pennant, 1777), from the Çanakkale Strait (Abidealtı), Turkey

2021 ◽  
Vol 50 (1) ◽  
pp. 16-23
Author(s):  
Bayram Kizilkaya ◽  
Sefa Acarli ◽  
Pervin Vural Ertuğrul ◽  
Selçuk Berber ◽  
Pınar Çelik
Keyword(s):  
Free Radicals ◽  
Antioxidant Capacity ◽  
Cell Damage ◽  
Nutrient Content ◽  
The Body ◽  
Dpph Radical ◽  
High Quality ◽  
Sweeping Effect ◽  
Metabolic Activities ◽  
Razor Clams

Abstract Metabolic activities such as breathing and digestion, resulting from natural functions of the body through oxidation, lead to the formation of free radicals that cause cancer, premature cardiac aging and some chronic diseases. Antioxidants are substances that remove free radicals and prevent cell damage. Seafood significantly contributes to the elimination of free radicals, especially owing to its high quality nutrient content. In this context, the objective of the study was to determine the radical antioxidant capacity and the total amount of carotenes in razor clams. The IC50 (mg g−1) value of the DPPH radical sweeping effect varied over the months (p < 0.05), showing the highest value in June, gradually decreasing from September and reaching the lowest level in February. The total amount of carotenoids also varied, with the highest value in September (p < 0.05). The total amount of chlorophyll ranged from 6.15 μg g−1 in August to 66.71 μg g−1 in December.

Curculigo orchioides Protects Cisplatin-Induced Cell Damage

2013 ◽  
Vol 41 (02) ◽  
pp. 425-441 ◽  
Author(s):  
Tong Ho Kang ◽  
Bin Na Hong ◽  
Su-Young Jung ◽  
Jeong-Han Lee ◽  
Hong-Seob So ◽  
...  
Keyword(s):  
Hydrogen Peroxide ◽  
Lipid Peroxidation ◽  
Hydroxyl Radicals ◽  
Cell Damage ◽  
Superoxide Radicals ◽  
Ros Generation ◽  
Protective Mechanism ◽  
Dependent Manner ◽  
Protective Effects ◽  
Curculigo Orchioides

Cisplatin is commonly used as a chemotherapeutic agent against many human cancers. However, it generates reactive oxygen species (ROS) and has serious dose-limiting side effects, including ototoxicity. The roots of Curculigo orchioides (C. orchioides) have been used to treat auditory diseases such as tinnitus and hearing loss in Chinese traditional medicine. In the present study, we investigated the protective effects of an ethanol extract obtained from C. orchioides rhizome (COR) on cisplatin-induced cell damage in auditory cells (HEI-OC1). COR (2.5–25 μg/ml) inhibited cisplatin-induced HEI-OC1 cell damage in a dose-dependent manner. To investigate the protective mechanism of COR on cisplatin cytotoxicity in HEI-OC1 cells, we measured the effects of COR on ROS generation and lipid peroxidation in cisplatin-treated cells as well as its scavenging activities against superoxide radicals, hydroxyl radicals, hydrogen peroxide, and DPPH radicals. COR (1–25 μg/ml) had scavenging activities against superoxide radicals, hydroxyl radicals, hydrogen peroxide, and DPPH radicals, as well as reduced lipid peroxidation. In in vivo experiments, COR was shown to reduce cochlear and peripheral auditory function impairments through cisplatin-induced auditory damage in mice. These results indicate that COR protects from cisplatin-induced auditory damage by inhibiting lipid peroxidation and scavenging activities against free radicals.

scholarly journals Blueberry Polyphenol Extracts Enhance the Intestinal Antioxidant Capacity in Weaned Rats by Modulating the Nrf2–Keap1 Signal Pathway

2021 ◽  
Vol 12 ◽  
Author(s):  
Fangfang Zhao ◽  
Shen Yan ◽  
Mengliang Tian
Keyword(s):  
Oxidative Stress ◽  
Antioxidant Capacity ◽  
Gene Transcription ◽  
Interleukin 1 ◽  
Antioxidant Properties ◽  
The Body ◽  
Initiation Factor ◽  
Standard Diet ◽  
Related Factor ◽  
Protective Effects

Weaning causes the generation of excessive reactive oxygen species in the body, which could lead to oxidative stress. Polyphenols, for which blueberries are an important dietary source, are known for various health benefits including antioxidant properties. Here, we sought to elucidate the effects of blueberry polyphenol extracts (BPE) on intestinal antioxidant capacity and possible underlying mechanisms in weaned rats. Ninety-six rats were assigned to two groups and fed either a standard diet or a standard diet supplemented with BPE (200 mg/kg). The results showed that BPE supplementation increased (P &lt; 0.05) catalase and superoxide dismutase activities and decreased (P &lt; 0.05) interleukin-1 and interferon-γ contents in the jejunum and ileum. The abundances of mammalian target of rapamycin, ribosomal p70 S6 kinase and eukaryotic initiation factor 4E-binding protein 1 mRNA were elevated in the jejunum and ileum (P &lt; 0.05) after BPE supplementation. Additionally, BPE supplementation decreased (P &lt; 0.05) Kelch-like ECH-associated protein 1 (Keap1) gene transcription and enhanced (P &lt; 0.05) NF-E2-related factor 2 (Nrf2) gene transcription in the jejunum and ileum. According to our results, BPE-induced protective effects against oxidative stress appear through the promotion of the jejunal and ileal antioxidant defense system in weaned rats, which was associated with the Nrf2–Keap1 signaling pathway.

scholarly journals The Protective Effects of α-Mangostin Attenuate Sodium Iodate-Induced Cytotoxicity and Oxidative Injury via Mediating SIRT-3 Inactivation via the PI3K/AKT/PGC-1α Pathway

Antioxidants ◽  
2021 ◽  
Vol 10 (12) ◽  
pp. 1870
Author(s):  
Chen-Ju Chuang ◽  
Meilin Wang ◽  
Jui-Hsuan Yeh ◽  
Tzu-Chun Chen ◽  
Shang-Chun Tsou ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Caspase 3 ◽  
Cell Damage ◽  
Outer Nuclear Layer ◽  
Retinal Pigment ◽  
Age Related Macular Degeneration ◽  
Dependent Manner ◽  
Protective Effects ◽  
Age Related

It is well known that age-related macular degeneration (AMD) is an irreversible neurodegenerative disease that can cause blindness in the elderly. Oxidative stress-induced retinal pigment epithelial (RPE) cell damage is a part of the pathogenesis of AMD. In this study, we evaluated the protective effect and mechanisms of alpha-mangostin (α-mangostin, α-MG) against NaIO3-induced reactive oxygen species (ROS)-dependent toxicity, which activates apoptosis in vivo and in vitro. MTT assay and flow cytometry demonstrated that the pretreatment of ARPE-19 cells with α-MG (0, 3.75, 7.5, and 15 μM) significantly increased cell viability and reduced apoptosis from NaIO3-induced oxidative stress in a concentration-dependent manner, which was achieved by the inhibition of Bax, cleaved PARP-1, cleaved caspase-3 protein expression, and enhancement of Bcl-2 protein. Furthermore, pre-incubation of ARPE-19 cells with α-MG markedly inhibited the intracellular ROS and extracellular H2O2 generation via blocking of the abnormal enzyme activities of superoxide dismutase (SOD), the downregulated levels of catalase (CAT), and the endogenous antioxidant, glutathione (GSH), which were regulated by decreasing PI3K-AKT-PGC-1α-STRT-3 signaling in ARPE-19 cells. In addition, our in vivo results indicated that α-MG improved retinal deformation and increased the thickness of both the outer nuclear layer and inner nuclear layer by inhibiting the expression of cleaved caspase-3 protein. Taken together, our results suggest that α-MG effectively protects human ARPE-19 cells from NaIO3-induced oxidative damage via antiapoptotic and antioxidant effects.

Neurobehavioral changes in mice offspring induced by prenatal exposure to acute toxicity of sodium selenite

Biologia ◽  
2011 ◽  
Vol 66 (2) ◽  
Author(s):  
Jamaan Ajarem ◽  
Gada Basher ◽  
Hossam Ebaid
Keyword(s):  
Atomic Absorption ◽  
Prenatal Exposure ◽  
Active Avoidance ◽  
Sodium Selenite ◽  
Essential Element ◽  
The Body ◽  
Control Group ◽  
Dependent Manner ◽  
Sensory Motor ◽  
Dose Dependent

AbstractSelenium is an essential element with a narrow margin between beneficial and toxic effects. This study was aimed to determine the neurobehavioral changes resulted from the prenatal exposure of mice to high doses of sodium selenite during fetal and early postnatal development. Atomic absorption for monitoring the placental transfer of selenium to offspring was employed. The developmental observations as well as the behavioral tests, such as sensory motor reflexes, and learning and memory test in automatic reflex conditioner (shuttle box) (active avoidance responses) were applied. Adult mice was assigned into three groups: the first group was remained as a control group given phosphate buffered saline; the second and the third groups were orally administrated sodium selenite at doses of 1 mg/kg and 4 mg/kg of the diet, respectively started from the 7th day to the end of the gestation period. Appearance of body hair and opening of eyes of the pups from treated mothers were delayed in a dose-dependent manner. The body weight gain came significantly lower than those of the control especially at the higher dose. Selenite also inhibited the sensory motor reflexes in all elements of acts and postures in a dose dependent manner. The active avoidance training-test indicated that selenite exposure was associated with learning impairment. Acetylcholine recorded a significant decrease in almost all the period of this study. By using atomic absorption, we found a significant high concentration of selenium in the brain, liver and kidney until the 40th postnatal day, indicating active transfer of selenium from mothers to embryos.

scholarly journals Catechin Treatment Ameliorates Diabetes and Its Complications in Streptozotocin-Induced Diabetic Rats

Dose-Response ◽  
2017 ◽  
Vol 15 (1) ◽  
pp. 155932581769115 ◽  
Author(s):  
Saeed Samarghandian ◽  
Mohsen Azimi-Nezhad ◽  
Tahereh Farkhondeh
Keyword(s):  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Experimental Period ◽  
Diabetic Rats ◽  
The Body ◽  
Lipoprotein Cholesterol ◽  
Dependent Manner ◽  
Protective Effects ◽  
Glutathione S Transferase ◽  
Apo B

Context: Diabetes mellitus causes atherosclerosis and lipid abnormalities. Hypolipidemic and antioxidative properties of catechin (CTN) have been reported in several studies. Objective: This study assesses the possible protective effects of CTN against oxidative damage in the diabetic rats. Materials and Methods: The rats were divided into the control, untreated diabetic, and 3 CTN-treated diabetic groups (20, 40, and 80 mg/kg/d, intraperitoneal). The diabetic rats were induced by streptozotocin. Catechin was injected for 4 weeks. At the end of the experimental period, glucose, lipid profile, apoprotein A-I (apo A-I), apoprotein B (apo B), malondialdehyde (MDA) levels, and antioxidant enzymes including glutathione- S-transferase (GST), superoxide dismutase (SOD), and catalase (CAT) activities were determined in serum. Statistical analyses were performed using the InStat 3.0 program. Results: Streptozotocin caused an elevation of glucose, MDA, triglycerides (TGs), total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C), and apo B with reduction in high-density lipoprotein cholesterol (HDL-C), apo A-I, SOD, CAT, and GST in the serum ( P < .05). The findings showed that the significant elevation in the body weight, glucose, MDA, TG, TC, LDL-C, and apo B and reduction in HDL-C, apo A-I, SOD, CAT, and GST were ameliorated in the CTN-treated diabetic groups versus the untreated group, in a dose-dependent manner ( P < .05). Conclusion: The present investigation proposes that CTN may ameliorate diabetes and its complications by modification of oxidative stress.

scholarly journals Sepsis and ARDS: The Dark Side of Histones

2015 ◽  
Vol 2015 ◽  
pp. 1-9 ◽  
Author(s):  
Zhiheng Xu ◽  
Yongbo Huang ◽  
Pu Mao ◽  
Jianrong Zhang ◽  
Yimin Li
Keyword(s):  
Neutralizing Antibodies ◽  
Cell Damage ◽  
Activated Protein C ◽  
Basic Structure ◽  
The Body ◽  
Dark Side ◽  
Protective Effects ◽  
Extracellular Histones ◽  
Physical Challenges

Despite advances in management over the last several decades, sepsis and acute respiratory distress syndrome (ARDS) still remain major clinical challenges and the leading causes of death for patients in intensive care units (ICUs) due to insufficient understanding of the pathophysiological mechanisms of these diseases. However, recent studies have shown that histones, also known as chromatin-basic structure proteins, could be released into the extracellular space during severe stress and physical challenges to the body (e.g., sepsis and ARDS). Due to their cytotoxic and proinflammatory effects, extracellular histones can lead to excessive and overwhelming cell damage and death, thus contributing to the pathogenesis of both sepsis and ARDS. In addition, antihistone-based treatments (e.g., neutralizing antibodies, activated protein C, and heparin) have shown protective effects and have significantly improved the outcomes of mice suffering from sepsis and ARDS. Here, we review researches related to the pathological role of histone in context of sepsis and ARDS and evaluate the potential value of histones as biomarkers and therapeutic targets of these diseases.

scholarly journals Protective Effects of Lemon Juice on Alcohol-Induced Liver Injury in Mice

2017 ◽  
Vol 2017 ◽  
pp. 1-8 ◽  
Author(s):  
Tong Zhou ◽  
Yu-Jie Zhang ◽  
Dong-Ping Xu ◽  
Fang Wang ◽  
Yue Zhou ◽  
...  
Keyword(s):  
Lipid Peroxidation ◽  
Liver Injury ◽  
Antioxidant Capacity ◽  
Lemon Juice ◽  
Antioxidant Enzyme Activities ◽  
Dependent Manner ◽  
Protective Effects ◽  
Histopathological Changes ◽  
Excessive Alcohol Consumption

Chronic excessive alcohol consumption (more than 40–80 g/day for males and more than 20–40 g/day for females) could induce serious liver injury. In this study, effects of lemon juice on chronic alcohol-induced liver injury in mice were evaluated. The serum biochemical profiles and hepatic lipid peroxidation levels, triacylglycerol (TG) contents, antioxidant enzyme activities, and histopathological changes were examined for evaluating the hepatoprotective effects of lemon juice in mice. In addition, the in vitro antioxidant capacities of lemon juice were determined. The results showed that lemon juice significantly inhibited alcohol-induced increase of alanine transaminase (ALT), aspartate transaminase (AST), hepatic TG, and lipid peroxidation levels in a dose-dependent manner. Histopathological changes induced by alcohol were also remarkably improved by lemon juice treatment. These findings suggest that lemon juice has protective effects on alcohol-induced liver injury in mice. The protective effects might be related to the antioxidant capacity of lemon juice because lemon juice showed in vitro antioxidant capacity.

scholarly journals Interleukin-27 Protects Cardiomyocyte-Like H9c2 Cells against Metabolic Syndrome: Role of STAT3 Signaling

2015 ◽  
Vol 2015 ◽  
pp. 1-10 ◽  
Author(s):  
Wei-Lian Phan ◽  
Yu-Tzu Huang ◽  
Ming-Chieh Ma
Keyword(s):  
Metabolic Syndrome ◽  
Cell Damage ◽  
Dependent Manner ◽  
Protective Effects ◽  
H9c2 Cells ◽  
Cytochrome C Release ◽  
Stat3 Signaling ◽  
Exogenous Treatment ◽  
Transcription 3

The present results demonstrated that high glucose (G), salt (S), and cholesterol C (either alone or in combination), as mimicking extracellular changes in metabolic syndrome, damage cardiomyocyte-like H9c2 cells and reduce their viability in a time-dependent manner. However, the effects were greatest when cells were exposed to all three agents (GSC). The mRNA of glycoprotein (gp) 130 and WSX-1, both components of the interleukin (IL)-27 receptor, were present in H9c2 cells. Although mRNA expression was not affected by exogenous treatment with IL-27, the expression of gp130 mRNA (but not that of WSX-1 mRNA) was attenuated by GSC. Treatment of IL-27 to H9c2 cells increased activation of signal transducer and activator of transcription 3 (STAT3) and protected cells from GSC-induced cytochrome c release and cell damage. The protective effects of IL-27 were abrogated by the STAT3 inhibitor, stattic. The results of the present study clearly demonstrate that the STAT3 pathway triggered by anti-inflammatory IL-27 plays a role in protecting cardiomyocytes against GSC-mediated damage.

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