scholarly journals Yes to “NO” host flora symbiosis

2016 ◽  
Vol 38 (5) ◽  
pp. 18-21 ◽  
Author(s):  
Alexandria Nichols ◽  
Khandaker A. Ahmed ◽  
Rakesh P. Patel
Keyword(s):  
Nitric Oxide ◽  
Free Radical ◽  
Redox Reactions ◽  
The Body ◽  
No Production ◽  
Targeted Therapeutics ◽  
Biological Functions ◽  
Health And Disease ◽  
Oxygen Tensions ◽  
Local Oxygen

Nitric oxide (NO) is a relatively simple molecule comprising only two atoms. Understanding how this free radical controls an array of complex biological functions provides the platform for much of the research in NO biochemistry and biology. Here, we discuss an updated perspective on how this gas is formed in the body involving a fascinating interplay between the diet, bacteria residing on the tongue, and redox reactions that are regulated by pH and local oxygen tensions. We highlight this as an area primed for novel microbe-targeted therapeutics for controlling NO production and affecting human health and disease.

scholarly journals Effect of Cadmium Exposure in Polymorphisms Gene NOS3, Blood Cadmium Level, Nitric Oxide Level, Blood Pressure and Antioxidant Enzymes

2018 ◽  
Vol 73 ◽  
pp. 06006
Author(s):  
Hernayanti ◽  
Santoso Slamet ◽  
Lestari Sri
Keyword(s):  
Nitric Oxide ◽  
Blood Pressure ◽  
Antioxidant Enzyme ◽  
Human Life ◽  
The Body ◽  
No Production ◽  
Textile Materials ◽  
Length Polymorphisms ◽  
Exposed Individual ◽  
Result Show

Cadmium is one of a heavy metal which widely used in human life, especially in the electroplating industry and a mixture of textile materials. Cadmium that enters the body binds to the metallothioneins protein. It can increase the formation of free radical compounds, there by inhibiting enzyme activity such as nitric oxide synthase3. This gene regulates the expression of endothelial nitric oxide synthase which produce a nitric oxide. Nitric oxide role in regulated blood pressure as vasodilator with Angiotensin II as vasoconstriction. The susceptibility to Cd exposure will elevate if the polymorphisms of gene is found in population. The aim of this research was to know effect of cadmium to gene NOS3 polymorphisms on NO, systolic and diastolic blood pressure and antioxidant enzyme in Cd-exposed individual. The genotype individual were detected by Polymerase Chain Reaction-Restriction Fragment Length Polymorphisms (PCR-RLFP) with MBo1 restriction enzyme. Parameter recorded were blood Cd , NO level, SOD, systolic and diastolic. Data were analyzed by independent t-test. These result showed that 20% of 40 individual of cases subject were detected as polymorphisms individual of NOS3gene, with GA genotype. Their fragment DNA located on 206 bp, 119 bp and 87 bp, but non polymorphisms of NO gene is only located on 206 bp. The result show cadmium could influence polymorphisms NOS3gene and decrease NO production followed by increasing of blood pressure both systolic and diastolic. Cadmium also decrease antioxidant enzyme SOD and GPx level.

scholarly journals Signalling Molecules in the Urothelium

2014 ◽  
Vol 2014 ◽  
pp. 1-14 ◽  
Author(s):  
Michael Winder ◽  
Gunnar Tobin ◽  
Daša Zupančič ◽  
Rok Romih
Keyword(s):  
Nitric Oxide ◽  
Urinary Bladder ◽  
Major Part ◽  
Current Knowledge ◽  
The Body ◽  
Present Review ◽  
Signalling Molecules ◽  
Ability To Act ◽  
Different Types ◽  
Health And Disease

The urothelium was long considered to be a silent barrier protecting the body from the toxic effects of urine. However, today a number of dynamic abilities of the urothelium are well recognized, including its ability to act as a sensor of the intravesical environment. During recent years several pathways of these urothelial abilities have been proposed and a major part of these pathways includes release of signalling molecules. It is now evident that the urothelium represents only one part of the sensory web. Urinary bladder signalling is finely tuned machinery of signalling molecules, acting in autocrine and paracrine manner, and their receptors are specifically distributed among different types of cells in the urinary bladder. In the present review the current knowledge of the formation, release, and signalling effects of urothelial acetylcholine, ATP, adenosine, and nitric oxide in health and disease is discussed.

scholarly journals Adiponectin, Obesity, and Cancer: Clash of the Bigwigs in Health and Disease

2019 ◽  
Vol 20 (10) ◽  
pp. 2519 ◽  
Author(s):  
Sheetal Parida ◽  
Sumit Siddharth ◽  
Dipali Sharma
Keyword(s):  
Cancer Progression ◽  
Protective Role ◽  
The Body ◽  
Biological Functions ◽  
Anti Cancer ◽  
Guardian Angel ◽  
Health And Disease ◽  
Obesity And Cancer ◽  
Multiple Signaling

Adiponectin is one of the most important adipocytokines secreted by adipocytes and is called a “guardian angel adipocytokine” owing to its unique biological functions. Adiponectin inversely correlates with body fat mass and visceral adiposity. Identified independently by four different research groups, adiponectin has multiple names; Acrp30, apM1, GBP28, and AdipoQ. Adiponectin mediates its biological functions via three known receptors, AdipoR1, AdipoR2, and T-cadherin, which are distributed throughout the body. Biological functions of adiponectin are multifold ranging from anti-diabetic, anti-atherogenic, anti-inflammatory to anti-cancer. Lower adiponectin levels have been associated with metabolic syndrome, type 2 diabetes, insulin resistance, cardiovascular diseases, and hypertension. A plethora of experimental evidence supports the role of obesity and increased adiposity in multiple cancers including breast, liver, pancreatic, prostrate, ovarian, and colorectal cancers. Obesity mediates its effect on cancer progression via dysregulation of adipocytokines including increased production of oncogenic adipokine leptin along with decreased production of adiponectin. Multiple studies have shown the protective role of adiponectin in obesity-associated diseases and cancer. Adiponectin modulates multiple signaling pathways to exert its physiological and protective functions. Many studies over the years have shown the beneficial effect of adiponectin in cancer regression and put forth various innovative ways to increase adiponectin levels.

scholarly journals Wound Healing Effect of Essential Oil Extracted from Eugenia dysenterica DC (Myrtaceae) Leaves

Molecules ◽  
2018 ◽  
Vol 24 (1) ◽  
pp. 2 ◽  
Author(s):  
Sandra Mazutti da Silva ◽  
Claudio Rezende Costa ◽  
Guilherme Martins Gelfuso ◽  
Eliete Silva Guerra ◽  
Yanna de Medeiros Nóbrega ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Cell Migration ◽  
Essential Oil ◽  
Cell Line ◽  
The Body ◽  
No Production ◽  
Cam Assay ◽  
Skin Cell ◽  
Natural Oils ◽  
Eugenia Dysenterica

The use of natural oils in topical pharmaceutical preparations has usually presented safe agents for the improvement of human health. Based on research into the immense potential of wound management and healing, we aimed to validate the use of topical natural products by studying the ability of the essential oil of Eugenia dysenterica DC leaves (oEd) to stimulate in vitro skin cell migration. Skin cytotoxicity was evaluated using a fibroblast cell line (L929) by MTT assay. The oil chemical profile was investigated by GC-MS. Moreover, the inhibition of lipopolysaccharide (LPS) induced nitric oxide (NO) production in the macrophage cell line (RAW 264.7) tested. The Chick Chorioallantoic Membrane (CAM) assay was used to evaluate the angiogenic activity and irritating potential of the oil. The oEd induces skin cell migration in a scratch assay at a concentration of 542.2 µg/mL. α-humulene and β-caryophyllene, the major compounds of this oil, as determined by GC-MS, may partly explain the migration effect. The inhibition of nitric oxide by oEd and α-humulene suggested an anti-inflammatory effect. The CAM assay showed that treatment with oEd ≤ 292 µg/mL did not cause skin injury, and that it can promote angiogenesis in vivo. Hence, these results indicate the feasibility of the essential oil of Eugenia dysenterica DC leaves to developed dermatological products capable of helping the body to repair damaged tissue.

scholarly journals Neuropeptide Y Reduces Nasal Epithelial T2R Bitter Taste Receptor–Stimulated Nitric Oxide Production

Nutrients ◽  
2021 ◽  
Vol 13 (10) ◽  
pp. 3392
Author(s):  
Ryan M. Carey ◽  
Nithin D. Adappa ◽  
James N. Palmer ◽  
Robert J. Lee
Keyword(s):  
Nitric Oxide ◽  
Neuropeptide Y ◽  
Bitter Taste ◽  
Beat Frequency ◽  
Taste Receptor ◽  
Ciliary Beat Frequency ◽  
Fluid Secretion ◽  
The Body ◽  
No Production ◽  
Neuropeptide Tyrosine

Bitter taste receptors (T2Rs) are G-protein-coupled receptors (GPCRs) expressed on the tongue but also in various locations throughout the body, including on motile cilia within the upper and lower airways. Within the nasal airway, T2Rs detect secreted bacterial ligands and initiate bactericidal nitric oxide (NO) responses, which also increase ciliary beat frequency (CBF) and mucociliary clearance of pathogens. Various neuropeptides, including neuropeptide tyrosine (neuropeptide Y or NPY), control physiological processes in the airway including cytokine release, fluid secretion, and ciliary beating. NPY levels and/or density of NPYergic neurons may be increased in some sinonasal diseases. We hypothesized that NPY modulates cilia-localized T2R responses in nasal epithelia. Using primary sinonasal epithelial cells cultured at air–liquid interface (ALI), we demonstrate that NPY reduces CBF through NPY2R activation of protein kinase C (PKC) and attenuates responses to T2R14 agonist apigenin. We find that NPY does not alter T2R-induced calcium elevation but does reduce T2R-stimulated NO production via a PKC-dependent process. This study extends our understanding of how T2R responses are modulated within the inflammatory environment of sinonasal diseases, which may improve our ability to effectively treat these disorders.

Abstract 335: Atheroma-specific Delivery of Synthetic High-density Lipoprotein Containing Sphingosine-1-phosphate for Modulation of Vascular Inflammation.

2015 ◽  
Vol 35 (suppl_1) ◽  
Author(s):  
Emily E Morin ◽  
Yanhong Guo ◽  
Rui Kuai ◽  
Gergely Lautner ◽  
Mark E Meyerhoff ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Endothelial Cells ◽  
Vascular Inflammation ◽  
The Body ◽  
Saline Control ◽  
No Production ◽  
No Release ◽  
Sphingosine 1 Phosphate ◽  
Anti Inflammatory

Introduction: Sphingosine-1-phosphate (S1P) is a potent anti-inflammatory signaling lipid carried in the body by circulating HDL. HDL has been shown to exhibit anti-inflammatory activities through activation of endothelial nitric oxide synthase (eNOS) and subsequent production and release of nitric oxide (NO) by endothelial cells. Objective: The aim of this study is to use synthetic HDL particles to selectively deliver S1P to the site of arterial plaques in order to exert anti-inflammatory activity and modulate the progression of atherosclerosis. Methods/Results: Synthetic HDL (sHDL) particles were prepared using the ApoA1 mimetic peptide 22A (PVLDLFRELLNELLEALKQKLK), dipalmitoylphosphatidylcholine (DPPC) and sphingomyelin. We also prepared sHDL containing either the hydrophobic dye, DiD, or S1P to assess the capability of sHDL to effectively reach atheroma site and induce nitric oxide (NO) release, respectively. The purity of all particles was determined to be > 97% and average particle size was 9.6 ± 0.4 nm for all preparations. To measure sHDL accumulation in the plaque, ApoE -/- mice were intravenously injected with 0.2 mg/kg HDL-DiD. Whole aortas were excised and analysed by IVUS imaging system, revealing significant accumulation of sHDL-DiD in the atherosclerotic lesions. We then tested the ability of sHDL to deliver S1P in vitro and induce NO production by treating human umbilical vein endothelial cells (HUVEC) with 1 mg/mL of 22A-DPPC-sHDL containing 0, 0.05, 0.5, or 5 nmol/mL of S1P using free 22A peptide (1 mg/mL) and saline as controls, and analyzing media by ozone chemiluminescence. Blank sHDL particles increased NO production two-fold over controls (0.27 ± 0.02 μM for 22A-DPPC-sHDLDL, 0.13 ± 0.01 μM PBS and 0.14 ± 0.02 μM for 22A peptide), while HDL-S1P further increased NO release: 0.35 ± 0.03, 0.44 ± 0.01, and 0.59 ± 0.01 μM for HDL with 0.05, 0.5, and 5 nmol/mL S1P, respectively. Conclusions: Our studies show that HDL is capable of delivering hydrophobic cargo to atherosclerotic plaques, making HDL a promising platform to deliver S1P for modulation vascular inflammation and atherosclerosis. In vitro studies have revealed that HDL-S1P is able to increase NO production 2 to 4-fold over saline control setting the basis for future in vivo studies.

Effect of culture Po2on macrophage (RAW 264.7) nitric oxide production

2001 ◽  
Vol 280 (2) ◽  
pp. C280-C287 ◽  
Author(s):  
Cynthia M. Otto ◽  
James E. Baumgardner
Keyword(s):  
Nitric Oxide ◽  
Cell Culture ◽  
Oxygen Tension ◽  
Inflammatory Responses ◽  
No Production ◽  
Inos Activity ◽  
Lower Oxygen ◽  
Oxygen Tensions

Macrophages are commonly cultured at a Po2of 149 Torr, but tissue macrophages in vivo live in an environment of much lower oxygen tension. Despite the many potential mechanisms for changes in oxygen tension to influence nitric oxide (NO) synthesis, there have been few reports investigating the effect of Po2on macrophage NO production. With the use of a culture chamber designed to rigorously control oxygen tension, we investigated the effects of culture Po2on macrophage NO production, inducible nitric oxide synthase (iNOS) activity, iNOS protein, and tumor necrosis factor production. NO production and iNOS activity were linearly related in the range of 39.4 to 677 Torr, but not in the range of 1.03 to 39.4 Torr. Therefore, results obtained in vitro for the high oxygen tensions commonly used in cell culture were quantitatively and qualitatively different from results obtained in cells cultured at the lower oxygen tensions that more accurately reflect the in vivo environment. The influence of oxygen tension on NO production has implications for cell culture methodology and for the relationship between microcirculatory dysfunction and inflammatory responses in rodent models of sepsis.

scholarly journals Antioxidant Activity and Probiotic Properties of Lactic Acid Bacteria

Fermentation ◽  
2022 ◽  
Vol 8 (1) ◽  
pp. 29
Author(s):  
Seonyoung Kim ◽  
Ji Yeon Lee ◽  
Yulah Jeong ◽  
Chang-Ho Kang
Keyword(s):  
Oxidative Stress ◽  
Nitric Oxide ◽  
Antioxidant Activity ◽  
Radical Scavenging ◽  
The Body ◽  
No Production ◽  
Probiotic Properties ◽  
Bacterial Strains ◽  
Inhibition Effect ◽  
Adhesion Ability

Oxidative stress, which can cause imbalance in the body by damaging cells and tissues, arises from the immoderate production of reactive oxygen species (ROS)/reactive nitrogen species (RNS). Therefore, external supplements having antioxidant activity are required for reducing oxidative stress. In our study, we investigated DPPH and ABTS radical scavenging ability, and the inhibition effect on the nitric oxide (NO) production of 15 food-derived bacterial strains in LPS-activated RAW264.7 cells. Among these LAB strains, eight strains with an excellent inhibition effect on NO production were selected through comparisons within the same genera. Moreover, the selected strains, including Leuconostoc mesenteroides MG860, Leu. citreum MG210, Pediococcus acidilactici MG5001, P. pentosaceus MG5078, Weissella cibaria MG5090, Levilactobacillus brevis MG5306, Latilactobacillus curvatus MG5020, and Latilactobacillus sakei MG5048 diminished the inducible nitric oxide synthase (iNOS)/cyclooxygenase-2 (COX-2) expression. In addition, the stability and adhesion ability of the eight LAB strains in the gastrointestinal tract were determined. In conclusion, the selected strains have potential as new probiotics with antioxidant effects.

scholarly journals Polyphenols in preventing endothelial dysfunction

2017 ◽  
Vol 71 (1) ◽  
pp. 0-0 ◽  
Author(s):  
Sylwia Biegańska-Hensoldt ◽  
Danuta Rosołowska-Huszcz
Keyword(s):  
Nitric Oxide ◽  
Blood Pressure ◽  
Endothelial Dysfunction ◽  
Oxidative Dna Damage ◽  
Developed Countries ◽  
The Body ◽  
No Production ◽  
C Reactive Protein ◽  
Rat Cardiomyocytes ◽  
Reactive Protein

One of the main causes of mortality in developed countries is atherosclerosis. The pathogenesis of atherosclerosis is associated with endothelial dysfunction. Consumption of food rich in natural antioxidants including polyphenols significantly improves endothelial cells functions.Polyphenols have a beneficial effect on the human body and play an important part in protecting the cardiovascular system. Polyphenols present in food have antioxidant, anti-inflammatory, antihypertensive, antithrombotic and antiproliferative properties. Catechins cause an increase in the activity of endothelial nitric oxide synthase (eNOS) and increased production of nitric oxide (NO) and decrease in blood pressure. Catechins also reduce platelet adhesion, lower the concentration of C-reactive protein and tumor necrosis factor alpha and interleukin-6. Resveratrol inhibits NADPH oxidase expression, increases the expression of eNOS and NO production as well as decreases the expression of proinflammatory cytokines, and also lowers the concentration of the soluble forms of adhesion molecules – sICAM-1 and sVCAM-1 in blood. Quercetin reduces the blood level of low density lipoprotein cholesterol, lowers blood pressure, reduces the concentration of C-reactive protein and F2-isoprostane level. Curcumin has antagonistic activity to homocysteine. Curcumin increases the expression of eNOS and reduces oxidative DNA damage in rat cardiomyocytes. Numerous attempts are taken for improving the bioavailability of polyphenols in order to increase their use in the body.

scholarly journals L-Citrulline Influences the Body Temperature, Heat Shock Response and Nitric Oxide Regeneration of Broilers Under Thermoneutral and Heat Stress Condition

2021 ◽  
Vol 12 ◽  
Author(s):  
Victoria A. Uyanga ◽  
Minghui Wang ◽  
Tian Tong ◽  
Jingpeng Zhao ◽  
Xiaojuan Wang ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Heat Stress ◽  
Heat Shock ◽  
Body Temperature ◽  
Mrna Expression ◽  
Heat Shock Response ◽  
Control Diet ◽  
The Body ◽  
No Production ◽  
Shock Response

Heat stress (HS) adversely affects several physiological responses in organisms, but the underlying molecular mechanisms involved are yet to be fully understood. L-Citrulline (L-Cit) is a nutraceutical amino acid that is gaining research interest for its role in body temperature regulation and nitric oxide synthesis. This study investigated whether dietary supplementation with L-Cit (1% of basal diet) could ameliorate the effects of acute HS on thermotolerance, redox balance, and inflammatory responses of broilers. Ross 308 broilers (288 chicks) were subjected to two environments; thermoneutral at 24°C (TNZ) or HS at 35°C for 5 h, and fed two diets; control or L-Cit. The results showed that HS increased the ear, rectal (RT), and core body (CBT) temperatures of broilers, along with higher respiratory rate. The RT and CBT readings were intermittently affected with time effect, whereas, L-Cit supplementation lowered the mean CBT than the control diet. Antioxidant assays showed that superoxide dismutase was increased during HS, while, catalase was promoted by L-Cit supplementation. In addition, L-Cit induced glutathione peroxidase activity compared to the control diet during HS. Hypothalamic heat shock protein (HSP)-90 was upregulated by HS, but L-Cit downregulated heat shock factor (HSF)-1, and HSP 60 mRNA expressions. HSF 3 mRNA expression was downregulated by L-Cit under TNZ condition. More so, HS increased the plasma nitric oxide (NO) concentration but lowered the total NO synthase (tNOS) activity. In contrast, L-Cit supplementation limited NO production but increased the tNOS activity. Arginase activity was increased in the control fed group during HS but L-Cit supplementation lowered this effect. The NOS-COX pathway was significantly affected under TNZ condition, since L-Cit supplementation downregulated the mRNA expression of iNOS-COX2 in the hypothalamus, and further reduced the serum PGE2 concentration. Together, these data indicates that L-Cit influenced the antioxidant defense, heat shock response and nitric oxide regeneration both under thermoneutral and HS conditions; and that L-Cit may be directly and/or indirectly involved in the central regulation of body temperature.

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