scholarly journals Antioxidant and Anti-Inflammatory Activities of Pomegranate (Punica granatum) onEimeria papillata-Induced Infection in Mice

2015 ◽  
Vol 2015 ◽  
pp. 1-7 ◽  
Author(s):  
Omar S. O. Amer ◽  
Mohamed A. Dkhil ◽  
Wafaa M. Hikal ◽  
Saleh Al-Quraishy
Keyword(s):  
Interleukin 1 ◽  
Punica Granatum ◽  
Economic Loss ◽  
Mrna Levels ◽  
Prevalent Disease ◽  
Total Antioxidant ◽  
Pomegranate Peel Extract ◽  
Oxide Synthase ◽  
Necrosis Factor ◽  
Inducible Nitric Oxide

Coccidiosis is the most prevalent disease causing widespread economic loss, especially in poultry farms. Here, we investigated the effects of pomegranate peel extract (PPE) on the outcome of coccidiosis caused byEimeria papillatain mice. The data showed that mice infected withE. papillataand treated with PPE revealed a significant decrease in the output of oocysts in their faeces by day 5 p.i. Infection also induced inflammation and injury of the jejunum. This was evidenced (i) as increases in reactive oxygen species, (ii), as increased neutrophils and decreased lymphocytes in blood (ii) as increased mRNA levels of inducible nitric oxide synthase (iNOS), Bcl-2 gene, and of the cytokines interferon gamma (IFN-γ), tumour necrosis factor-α(TNF-α), and interleukin-1β(IL-1β), and (iv) as downregulation of mucin gene MUC2 mRNA. All these infection-induced parameters were significantly altered during PPE treatment. In particular, PPE counteracted theE. papillata-induced loss of the total antioxidant capacity. Our data indicated that PPE treatment significantly attenuated inflammation and injury of the jejunum induced byE. papillatainfections.

scholarly journals Alimentary induced fatty liver and adjuvant therapy with effective natural bioactive molecules

2011 ◽  
Vol 152 (26) ◽  
pp. 1035-1042 ◽  
Author(s):  
Viktor Hegedüs ◽  
Domokos Gerő ◽  
Zoltán Mihály ◽  
Attila Szijártó ◽  
Tivadar Zelles ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Fatty Liver ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Redox Homeostasis ◽  
Mrna Levels ◽  
Factor Α ◽  
Oxide Synthase ◽  
Necrosis Factor ◽  
Inducible Nitric Oxide

Changes of redox-homeostasis generate cytokines, and free radicals influence many intracellular signaling pathways in different liver diseases. Liophylised table beet and carrot powder (GPS Powder Kft. 1361/004/2003BFÁÉÉÁ) containing bioactive components such as betaine, betanins, betaxanthins, flavonoids, polyphenols, glutamine, beta carotene, vitamins and folic acid may produce changes various cellular pathways. Aim: The aim of this study was to determine the protecting effects of bioactive agents of the liophylised table beet and carrot powder on fatty liver in a “short term” experiment. Method: Male Wistar rats were fed with chow with or without high fat (2% cholesterol, 0.5% cholic acid, 20% sunflower oil) and treated with 0.1 or 1 g/bwkg/day natural product for ten days parallel with the feedings. Cyclooxygenase-2, inducible nitric oxide synthase and tumor necrosis factor-α mRNA levels were determined using molecular biologic methods. Free radicals, H-donating activity, reducing power and free SH-group concentrations were determined by luminometry and spectrophotometry. Mobilized methyl groups were assayed by over pressure liquid chromatography method in liver homogenates. Results: It was found that the higher dose of the natural product better decreased the induced free radical reactions, cyclooxygenase-2, inducible nitric oxide synthase and tumor necrosis factor-α mRNA-levels both in normal and fatty liver tissues. Although treatments failed to exert significant changes in all global antioxidant parameters, mobilized methyl group concentrations were higher after treatments in fatty liver. Favorable tendencies were also noted in the redox-homeostasis of the fatty liver after treatment. Conclusions: As expected, lyophylised table beet and carrot proved to be a “functional food” in rats with alimentary fat induced fatty liver. It cannot be ruled out that this beneficial effect may have clinical relevance. Orv. Hetil., 2011, 152, 1035–1042.

Roles of IL-1 and TNF in the decreased ileal muscle contractility induced by lipopolysaccharide

1999 ◽  
Vol 276 (6) ◽  
pp. G1356-G1362 ◽  
Author(s):  
Robert F. Lodato ◽  
A. Rizwan Khan ◽  
Malgorzata J. Zembowicz ◽  
Norman W. Weisbrodt ◽  
Thomas A. Pressley ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Smooth Muscle ◽  
Interleukin 1 ◽  
Smooth Muscle Contraction ◽  
Muscle Contractility ◽  
Gastrointestinal Stasis ◽  
Factor Α ◽  
Oxide Synthase ◽  
Necrosis Factor ◽  
Inducible Nitric Oxide

Gastrointestinal stasis during sepsis may be associated with gastrointestinal smooth muscle dysfunction. Endotoxin [lipopolysaccharide (LPS)] impairs smooth muscle contraction, in part through inducible nitric oxide synthase (NOS II) and enhanced nitric oxide production. We studied the roles of tumor necrosis factor-α (TNF) and interleukin-1 (IL-1) in this process by using TNF binding protein (TNFbp) and IL-1 receptor antagonist (IL-1ra). Rats were treated with TNFbp and IL-1ra, or their vehicles, 1 h before receiving LPS or saline. At 5 h after LPS, contractility was measured in strips of ileal longitudinal smooth muscle, and NOS II activity was measured in full-thickness segments of ileum. LPS decreased maximum stress (mean ± SE) from 508 ± 55 (control) to 355 ± 33 g/cm2( P < 0.05). Pretreatment with TNFbp plus IL-1ra prevented the LPS-induced decrease. Separate studies of TNFbp alone or IL-1ra alone indicated that, at the doses and timing used, TNFbp was more effective. LPS also increased NOS II activity by >10-fold ( P < 0.01) over control. This increase was prevented by TNFbp plus IL-1ra ( P = not significant vs. control). We conclude that the LPS-induced increase in NOS II activity and the decrease in ileal muscle contractility are mediated by TNF and IL-1.

scholarly journals Diethylcarbamazine Attenuates the Development of Carrageenan-Induced Lung Injury in Mice

2014 ◽  
Vol 2014 ◽  
pp. 1-12 ◽  
Author(s):  
Edlene Lima Ribeiro ◽  
Karla Patricia de Souza Barbosa ◽  
Ingrid Tavares Fragoso ◽  
Mariana Aragão Matos Donato ◽  
Fabiana Oliveira dos Santos Gomes ◽  
...  
Keyword(s):  
Acute Inflammation ◽  
Pleural Cavity ◽  
Interleukin 1 ◽  
Polymorphonuclear Cells ◽  
Inflammation Markers ◽  
Acute Lung Inflammation ◽  
Anti Inflammatory ◽  
Oxide Synthase ◽  
Necrosis Factor ◽  
Inducible Nitric Oxide

Diethylcarbamazine (DEC) is an antifilarial drug with potent anti-inflammatory properties as a result of its interference with the metabolism of arachidonic acid. The aim of the present study was to evaluate the anti-inflammatory activity of DEC in a mouse model of acute inflammation (carrageenan-induced pleurisy). The injection of carrageenan into the pleural cavity induced the accumulation of fluid containing a large number of polymorphonuclear cells (PMNs) as well as infiltration of PMNs in lung tissues and increased production of nitrite and tumor necrosis factor-αand increased expression of interleukin-1β, cyclooxygenase (COX-2), and inducible nitric oxide synthase. Carrageenan also induced the expression of nuclear factor-κB. The oral administration of DEC (50 mg/Kg) three days prior to the carrageenan challenge led to a significant reduction in all inflammation markers. The present findings demonstrate that DEC is a potential drug for the treatment of acute lung inflammation.

scholarly journals Inducible Nitric Oxide Synthase Is Not Essential for Control of Trypanosoma cruzi Infection in Mice

2004 ◽  
Vol 72 (7) ◽  
pp. 4081-4089 ◽  
Author(s):  
Kara L. Cummings ◽  
Rick L. Tarleton
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Trypanosoma Cruzi ◽  
Inducible Nitric Oxide Synthase ◽  
Interleukin 1 ◽  
Mouse Strains ◽  
Wild Type ◽  
Necrosis Factor Alpha ◽  
Oxide Synthase ◽  
Inducible Nitric Oxide

ABSTRACT Immune control of many intracellular pathogens, including Trypanosoma cruzi, is reported to be dependent on the production of nitric oxide. In this study, we show that mice deficient in inducible nitric oxide synthase (iNOS or NOS2) exhibit resistance to T. cruzi infection that is comparable to that of wild-type mice. This is the case for two iNOS-deficient mouse strains, Nos2tm1Lau and Nos2 N5, infected with the Brazil or Tulahuen strain of T. cruzi. In all cases, blood parasitemia, tissue parasite load, and survival rates are similar between wild-type and iNOS-deficient mice. In contrast, both wild-type and Nos2tm1Lau mice died within 32 days postinfection when treated with the nitric oxide synthase inhibitor aminoguanidine. Increased transcription of NOS1 or NOS3 is not found in iNOS-knockout (KO) mice, indicating that the absence of nitric oxide production through iNOS is not compensated for by increased production of other NOS isoforms. However, Nos2tm1Lau mice exhibit enhanced expression of tumor necrosis factor alpha, interleukin-1, and macrophage inflammatory protein 1α compared to that of wild-type mice, and these alterations may in part compensate for the lack of iNOS. These results clearly show that iNOS is not required for control of T. cruzi infection in mice.

scholarly journals Effects of Immunomodulatory Substances on Phagocytosis of A by Human Microglia

2010 ◽  
Vol 2010 ◽  
pp. 1-18 ◽  
Author(s):  
Erik Hjorth ◽  
Dan Frenkel ◽  
Howard Weiner ◽  
Marianne Schultzberg
Keyword(s):  
Nitric Oxide ◽  
Membrane Protein ◽  
Inducible Nitric Oxide Synthase ◽  
Inflammatory Markers ◽  
Interleukin 1 ◽  
Type I ◽  
Human Microglia ◽  
Amyloid A ◽  
Oxide Synthase ◽  
Inducible Nitric Oxide

Glial activation and increased inflammation characterize neuropathology in Alzheimer's disease (AD). The aim was to develop a model for studying phagocytosis of -amyloid (A) peptide by human microglia and to test effects thereupon by immunomodulatory substances. Human CHME3 microglia showed intracellular A colocalized with lysosome-associated membrane protein-2, indicating phagocytosis. This was increased by interferon-, and to a lesser degree with Protollin, a proteosome-based adjuvant. Secretion of brain-derived neurotrophic factor (BDNF) was decreased by A and by interferon- and interleukin-1. These cytokines, but not A, stimulated interleukin-6 release. Microglia which phagocytosed A exhibited a higher degree of expression of interleukin-1 receptor type I and inducible nitric oxide synthase. In conclusion, we show that human microglia are able to phagocytose A and that this is associated with expression of inflammatory markers. A and interferon- decreased BDNF secretion suggesting a new neuropathological role for A and the inflammation accompanying AD.

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