scholarly journals Equol Inhibits LPS-Induced Oxidative Stress and Enhances the Immune Response in Chicken HD11 Macrophages

2015 ◽  
Vol 36 (2) ◽  
pp. 611-621 ◽  
Author(s):  
Zhongyong Gou ◽  
Shouqun Jiang ◽  
Chuntian Zheng ◽  
Zhimei Tian ◽  
Xiajing Lin
Keyword(s):  
Oxidative Stress ◽  
Immune Response ◽  
Superoxide Dismutase ◽  
Glutathione Transferase ◽  
Interleukin 1 ◽  
Interleukin 2 ◽  
Transcript Abundance ◽  
Necrosis Factor Alpha ◽  
Factor Alpha ◽  
Oxide Synthase

Background/Aims: There has been increasing recent attention on the antioxidative capacity of equol. This study tested the effect of equol on oxidative stress induced by lipopolysaccharide (LPS) and regulation of immunity in chicken macrophages. Methods: Chicken HD11 macrophages were challenged with LPS (100 ng/mL) alone or with LPS (100 ng/mL) and (±)equol (10, 20, 40, 80, 160 μmol/L) together for 24h. Evaluated responses included the contents of malondialdehyde (MDA) and reduced glutathione (GSH), activities of total superoxide dismutase (T-SOD) and inducible nitric oxide synthase (iNOS), transcript abundance of superoxide dismutase 2 (SOD2), catalase (CAT), glutathione transferase (GST), Toll-like receptor 4 (TLR4), tumor necrosis factor alpha (TNFα) and interleukin-1 beta (IL-1β), and contents of the cytokines TNFα, IL-1β, interleukin-2 (IL-2) and interferon beta (IFNβ). Results: Exposure to LPS induced oxidative stress as contents of MDA increased and GSH decreased in LPS-treated cells (P < 0.05) compared to those in control cells. Compared to LPS alone, co-treatment with equol (20 μmol/L, 40 μmol/L or 80 μmol/L) reduced contents of MDA and increased those of GSH (both P < 0.05). Activity of T-SOD increased (P < 0.05) in cells treated with the higher contentration of equol (80 μmol/L or 160 μmol/L), however, all concentrations (20 μmol/L to 160 μmol/L) increased activity of iNOS (P < 0.05). The highest concentration of equol (160 μmol/L) increased SOD2 and GST transcripts (P < 0.05). Equol treatment increased transcripts of TLR4, TNFα and IL-1β (P < 0.05). And there were similar changes in contents of IL-1β, IL-2, IFNβ and TNFα in the cells (P < 0.05). Conclusions: It concluded that equol can protect chicken HD11 macrophages from oxidative stress induced by LPS through reducing lipid peroxidation products and enhancing contents of antioxidants, and activities of relevant antioxidase enzymes; effects were also seen in gene expression related to the immune response and increased contents of cytokines. The optimal concentration of equol on antioxidation and immune enhancement in chicken macrophages was 40 μmol/L.

scholarly journals Glycine and Selenium (Separately and in Combination) Reduced Bromate-Mediated Oxidative Stress and Inflammatory Response in U937 Cells

2020 ◽  
pp. 8-16
Author(s):  
Tebekeme Okoko
Keyword(s):  
Oxidative Stress ◽  
Nitric Oxide ◽  
Superoxide Dismutase ◽  
Interleukin 1 ◽  
Tumour Necrosis Factor Alpha ◽  
U937 Cells ◽  
Necrosis Factor Alpha ◽  
Factor Alpha ◽  
And Oxidative Stress ◽  
Necrosis Factor

The toxicity of bromate is ascribed to DNA damage and alteration in carbohydrate mechanism that could result to lipid peroxidation and oxidative stress. The effects of glycine and selenium on bromate-induced alterations on U937 cells and U937-derived macrophages were investigated. In the first experiment, U937 cells were incubated with or without glycine or selenium or both before subjecting cells to bromate exposure. Cell viability and production of ROS were assessed via MTT and DCHF-DA assays. In the other experiment, U937 cells were transformed to the macrophage form using phorbol 12-myristate 13-acetate before incubating with or without glycine and selenium before exposure to bromate. Secretion of nitric oxide and cytokines (tumour necrosis factor-alpha, interleukin 1 and interleukin 6) were later measured. The production of superoxide dismutase and catalase was also evaluated. The results revealed that bromate caused significant cytotoxicity and ROS production that was reduced when cells were pre-incubated by glycine and selenium (both separately and in combination). Bromate also increased macrophage secretion of nitric oxide and cytokines which was reduced by glycine and selenium. Bromate also suppressed the production of superoxide dismutase and catalase which was reversed by glycine and selenium (both separately and in combination) close to control values. The effects of glycine and selenium are ascribed to their antioxidant nature. Implications of the findings are discussed.

Nuclear Factor κB and Anesthetic Preconditioning during Myocardial Ischemia-Reperfusion

2004 ◽  
Vol 100 (3) ◽  
pp. 540-546 ◽  
Author(s):  
Caiyun Zhong ◽  
Yamei Zhou ◽  
Hong Liu
Keyword(s):  
Ischemia Reperfusion ◽  
Interleukin 1 ◽  
Intercellular Adhesion Molecule ◽  
Nuclear Factor ◽  
Intercellular Adhesion Molecule 1 ◽  
Necrosis Factor Alpha ◽  
Factor Alpha ◽  
Nf Kappab ◽  
Myocardial Ischemia Reperfusion ◽  
Oxide Synthase

Background Volatile anesthetic preconditioning (APC) protects against myocardial ischemia-reperfusion (IR) injury, but the precise mechanisms underlying this phenomenon remain undefined. To investigate the molecular mechanism of APC in myocardial protection, the activation of nuclear factor (NF) kappaB and its regulated inflammatory mediators expression were examined in the current study. Methods Hearts from male rats were isolated, Langendorff perfused, and randomly assigned to one of three groups: (1) the control group: hearts were continuously perfused for 130 min; (2) the IR group: 30 min of equilibration, 15 min of baseline, 25 min of ischemia, 60 min of reperfusion; and (3) the APC + IR group: 30 min of equilibration, 10 min of sevoflurane exposure and a 5-min washout, 25 min of global ischemia, 60 min of reperfusion. Tissue samples were acquired at the end of reperfusion. NF-kappaB activity was determined by electrophoretic mobility shift assay. The NF-kappaB inhibitor, IkappaB-alpha, was determined by Western blot analysis. Myocardial inflammatory mediators, including tumor necrosis factor alpha, interleukin 1, intercellular adhesion molecule 1, and inducible nitric oxide synthase, were also assessed by Western blot analysis. Results Nuclear factor kappaB-DNA binding activity was significantly increased at the end of reperfusion in rat myocardium, and cytosolic IkappaB-alpha was decreased. Supershift assay revealed the involvement of NF-kappaB p65 and p50 subunits. APC with sevoflurane attenuated NF-kappaB activation and reduced the expression of tumor necrosis factor alpha, interleukin 1, intercellular adhesion molecule 1, and inducible nitric oxide synthase. APC also reduced infarct size and creatine kinase release and improved myocardial left ventricular developed pressure during IR. Conclusions The results of this study indicate that attenuation of NF-kappaB activation and subsequent down-regulation of NF-kappaB-dependent inflammatory gene expression plays an important role in the protective mechanism of APC against acute myocardial IR injury.

scholarly journals Melatonin Alleviated Potassium Dichromate-Induced Oxidative Stress and Reprotoxicity in Male Rats

2021 ◽  
Vol 2021 ◽  
pp. 1-12
Author(s):  
Samir A. E. Bashandy ◽  
Hossam Ebaid ◽  
Jameel Al-Tamimi ◽  
Omar A.-H. Ahmed-Farid ◽  
Enayat A. Omara ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Superoxide Dismutase ◽  
Sperm Count ◽  
Potassium Dichromate ◽  
Reproductive Toxicity ◽  
Male Rats ◽  
Control Group ◽  
Necrosis Factor Alpha ◽  
Melatonin Administration ◽  
Factor Alpha

Melatonin (ML) is a potent antioxidant that reduces oxidative stress. This study was designed to examine the protective effect of melatonin on potassium dichromate- (PDC-) induced male reproductive toxicity. Forty rats were divided into five groups: the control group, rats administered PDC orally (10 mg/kg body weight) for eight weeks, rats administered ML intraperitoneally at doses of either 2.5 or 5 mg/kg followed by the administration of PDC, and rats administered 5 mg/kg ML only. The treatment of rats with PDC led to a decrease in the levels of plasma sex hormones, glutathione, superoxide dismutase, catalase, carnitine, sperm count, and motility. Testicular malondialdehyde levels, nitric oxide concentrations, and abnormalities increased significantly in the PDC group. Melatonin administration to the PDC-treated rats reduced the increase of malondialdehyde and restored the activity of antioxidant enzymes (superoxide dismutase and catalase), glutathione, and sex hormone levels. Moreover, ML attenuated PDC-induced increase in levels of tumor necrosis factor-alpha or interleukin-6. ML alleviated histopathological changes and an increase of p53-positive immune reaction due to PDC. Furthermore, ML inhibited PDC-induced decrease in the DNA content of spermatogenic cells. This study proposed that melatonin may be useful in mitigating oxidative stress-induced testicular damage due to potassium dichromate toxicity.

scholarly journals Influence of Vector-Encoded Cytokines on Anti-Salmonella Immunity: Divergent Effects of Interleukin-2 and Tumor Necrosis Factor Alpha

2001 ◽  
Vol 69 (6) ◽  
pp. 3980-3988 ◽  
Author(s):  
Basel K. al-Ramadi ◽  
Mariam H. Al-Dhaheri ◽  
Nada Mustafa ◽  
Mounir AbouHaidar ◽  
Damu Xu ◽  
...  
Keyword(s):  
Immune Response ◽  
Tumor Necrosis Factor ◽  
Tumor Necrosis Factor Alpha ◽  
Tumor Necrosis ◽  
Interleukin 2 ◽  
Fine Tuning ◽  
Necrosis Factor Alpha ◽  
Tnf Α ◽  
Factor Alpha ◽  
Necrosis Factor

ABSTRACT Attenuated Salmonella strains are of interest as new vaccine candidates and as vectors of cloned genes of other organisms. Attenuated strains expressing specific cytokines were constructed as a means of manipulating the immune response in various disease settings. In the present study, interleukin-2 (IL-2)-expressing (GIDIL2) or tumor necrosis factor alpha (TNF-α)-expressing (GIDTNF) strains were compared with the parent strain (BRD509) for the effect of cytokines on anti-Salmonella immunity. Expression of IL-2 resulted in a rapid clearance of the organism soon after vaccination. The reduction in GIDIL2 CFU was 50- to 300-fold higher than that of BRD509 and correlated with a markedly decreased splenomegaly. Furthermore, no evidence for any significant activation, including upregulation of surface markers and production of nitric oxide (NO), was observed in spleens of GIDIL2-injected mice. In contrast, the host response to GIDTNF was marked by an early, strong, splenic cellular influx, but surprisingly, the degree of induced splenomegaly and NO secretion was only 50% of that observed in BRD509-treated mice. Despite this, bacterial colonization of the spleen in GIDTNF-immunized animals was either slightly decreased from or equivalent to that of the BRD509-treated group, suggesting the induction of additional antimicrobial mechanisms by TNF-α. In vivo protection studies demonstrated that, at limiting doses, GIDIL2 was inferior to GIDTNF and BRD509 in its capacity to protect against virulent challenge. At high doses, however, all three strains exhibited equal protective efficacy. These results demonstrate that the immune response against intracellular bacteria can be manipulated by pathogen-expressed cytokines and open the way for further fine tuning of immune responses not only to Salmonella strains themselves but also to the heterologous gene(s) carried by them.

scholarly journals Effects of Selenium-Enriched Protein fromGanoderma lucidumon the Levels of IL-1βand TNF-α, Oxidative Stress, and NF-κB Activation in Ovalbumin-Induced Asthmatic Mice

2014 ◽  
Vol 2014 ◽  
pp. 1-6 ◽  
Author(s):  
Guan Min-chang ◽  
Tang Wei-hong ◽  
Xu Zhen ◽  
Sun Jie
Keyword(s):  
Oxidative Stress ◽  
Interleukin 1 ◽  
Experimental Conditions ◽  
Necrosis Factor Alpha ◽  
Organic Selenium ◽  
Inorganic Selenium ◽  
Tnf Α ◽  
Liver And Kidney ◽  
Factor Alpha ◽  
Endogenous Antioxidant

The purpose of this study was to compare the effect and toxicity of organic selenium (Pro-Se) with inorganic selenium (IOSe) in preventing asthma in ovalbumin-induced asthmatic mice. After the mice were treated orally with Pro-Se and IOSe, respectively, the plasma Se levels, Se accumulation in liver and kidney, tumor necrosis factor alpha (TNF-α), interleukin 1 beta (IL-1β), oxidative stress, and NF-κB activation in lung were examined. The results showed that the serumal Se levels in the mice fed the Pro-Se were significant (P<0.01) elevations. It results in restoration of the level of endogenous antioxidant enzyme, lower levels of TNF-αand IL-1β, and activated NF-κB in the asthmatic mice. Our experiments have demonstrated profound differences between the activities of organic selenium and inorganic selenium in experimental conditions. These data provide an important proof of the concept that organic selenium might be a new potential therapy for the management of childhood asthma in humans.

scholarly journals Nephroprotective Role of Beta vulgaris L. Root Extract against Chlorpyrifos-Induced Renal Injury in Rats

2019 ◽  
Vol 2019 ◽  
pp. 1-9 ◽  
Author(s):  
Gadah Albasher ◽  
Rafa Almeer ◽  
Saud Alarifi ◽  
Saad Alkhtani ◽  
Manal Farhood ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Organophosphorus Pesticides ◽  
Interleukin 1 ◽  
Renal Tissue ◽  
Root Extract ◽  
Health Issues ◽  
Necrosis Factor Alpha ◽  
Antioxidant Agents ◽  
Factor Alpha ◽  
Oxide Synthase

Organophosphorus pesticides (OPs) are widely used for agricultural and housekeeping purposes. Exposure to OPs is associated with the progression of several health issues. Antioxidant agents may be powerful candidates to minimise adverse reactions caused by OPs. The aim of the present study was to evaluate the nephroprotective effects of red beetroot extract (RBR) against chlorpyrifos- (CPF-) induced renal impairments. CPF induced kidney dysfunction, as demonstrated by changes in serum creatinine and urea levels. Moreover, CPF exposure induced oxidative stress in the kidneys as determined by increased malondialdehyde and nitric oxide levels, decreased glutathione content, decreased catalase, superoxide dismutase, glutathione peroxidase, and glutathione reductase activities, and decreased nuclear factor (erythroid-derived 2)-like-2 factor expression. In addition, CPF induced inflammation in renal tissue as evidenced by increased release of tumor necrosis factor-alpha and interleukin-1β and upregulation of inducible nitric oxide synthase. Furthermore, CPF promoted cell death as demonstrated by decreased Bcl-2 and increased Bax and caspase-3 levels. Treatment with RBR one hour prior to CPF treatment blocked the effects observed in response to CPF alone. Our results suggest that RBR could be used to alleviate CPF-induced nephrotoxicity through antioxidant, anti-inflammatory, and antiapoptotic activities.

IL-6 enhances TNF-alpha- and IL-1-induced increase of Mn superoxide dismutase mRNA and O2 tolerance

1992 ◽  
Vol 263 (1) ◽  
pp. L22-L26 ◽  
Author(s):  
M. F. Tsan ◽  
J. E. White ◽  
P. J. Del Vecchio ◽  
J. B. Shaffer
Keyword(s):  
Superoxide Dismutase ◽  
Endothelial Cell ◽  
Interleukin 1 ◽  
Tnf Alpha ◽  
Mrna Levels ◽  
Sod Activity ◽  
Necrosis Factor Alpha ◽  
Factor Alpha ◽  
Tracheal Insufflation

Tumor necrosis factor-alpha (TNF-alpha), interleukin-1 alpha (IL-1), and interleukin-6 (IL-6) are multifunctional cytokines produced by a number of cells in response to endotoxin. We have previously demonstrated (M.-F. Tsan, J. E. White, T. A. Santana, and C. Y. Lee. J. Appl. Physiol. 68: 1211–1219, 1990, and M.-F. Tsan, C. Y. Lee, and J. E. White. J. Appl. Physiol. 71: 688–697, 1991) that tracheal insufflation of 5 micrograms of TNF-alpha or 1 microgram of IL-1 markedly protects rats against O2 toxicity and enhances pulmonary Mn superoxide dismutase (Mn SOD) activity. We now report that TNF-alpha and IL-1 at subprotective doses, e.g., 1 and 0.2 micrograms, respectively, act synergistically in protecting rats against O2 toxicity. Likewise, TNF-alpha and IL-1 at 0.005 microgram/ml each act synergistically in enhancing endothelial cell Mn SOD, but not Cu,Zn SOD mRNA levels. IL-6 at 5 or 10 micrograms provides no protective effect in rats against O2 toxicity and at up to 0.5 microgram/ml has no apparent effect on endothelial cell Mn or Cu,Zn SOD mRNA levels. However, IL-6 markedly enhances TNF-alpha- and IL-1-induced increases in Mn SOD mRNA levels and O2 tolerance. These results support an important role of Mn SOD in the protection against O2 toxicity.

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