scholarly journals Study the effect of indomethacin administration on breast tumor growth and iNOS gene expression in tumor-bearing mice

2019 ◽  
Vol 7 (2) ◽  
pp. 172-184
Keyword(s):  
Gene Expression ◽  
Tumor Growth ◽  
Breast Tumor ◽  
Tumor Bearing ◽  
Inos Gene ◽  
Inos Gene Expression

scholarly journals Anti-Inflammatory Effects of Abeliophyllum distichum Nakai (Cultivar Okhwang 1) Callus through Inhibition of PI3K/Akt, NF-κB, and MAPK Signaling Pathways in Lipopolysaccharide-Induced Macrophages

Processes ◽  
2021 ◽  
Vol 9 (6) ◽  
pp. 1071
Author(s):  
Tae-Won Jang ◽  
Jae-Ho Park
Keyword(s):  
Gene Expression ◽  
Polymerase Chain Reaction ◽  
Signaling Pathways ◽  
Chain Reaction ◽  
Inos Gene ◽  
Polymerase Chain ◽  
Cox 2 ◽  
Anti Inflammatory ◽  
Abeliophyllum Distichum ◽  
Inos Gene Expression

One of the Korean endemic plants, Abeliophyllum distichum Nakai (Oleaceae), contains acteoside, which is a glycoside exhibiting neuroprotective, anti-inflammation effects and antibacterial capacities. We conducted an investigation on the effects of the callus of A. distichum (cultivar Okhwang 1, CAO) on pro-inflammatory mediators released following nuclear factor-кB (NF-кB), phosphatidylinositol 3-kinase/Akt (PI3K-Akt) and mitogen-activated protein kinase (MAPK) signal activation in lipopolysaccharide (LPS)-induced RAW 264.7 cells. Immunoblotting was employed to find out the expression of cyclooxygenase-2 (COX-2), inducible nitric oxide (iNOS), and activation of MAPK molecules, NF-κB and Akt. Cytokines, COX-2, and iNOS gene expression were assessed using polymerase chain reaction techniques. Cytokines, COX-2, and iNOS gene expression were assessed using polymerase chain reaction techniques. High-performance liquid chromatography revealed that CAO was rich in acteoside and isoacteoside. As a result, CAO inhibited the generation of NO, cytokines, COX-2, and iNOS expression. Further, translocation to the nuclear of NF-κB p65 and degradation of the inhibitor of NF-кB (IкB) were alleviated by suppressing phosphorylation. Additionally, CAO significantly impacted MAPK pathway activation by potentially reducing phosphorylation of MAPKs. These results indicate that the anti-inflammatory effect of CAO is mediated via the inhibition of MAPK, PI3K/Akt, and NF-κB signaling pathways, probably via glycosides, phenolics, and flavonoids bioactivity derived from plants. CAO can serve as a potential anti-inflammatory agent, which alleviates inflammation factors and act through specific cell signaling pathways.

PPARγ is not required for the inhibitory actions of PGJ2 on cytokine signaling in pancreatic β-cells

2004 ◽  
Vol 286 (3) ◽  
pp. E329-E336 ◽  
Author(s):  
Sarah M. Weber ◽  
Anna L. Scarim ◽  
John A. Corbett
Keyword(s):  
Gene Expression ◽  
Nitric Oxide ◽  
Cytokine Signaling ◽  
Rinm5f Cells ◽  
Β Cells ◽  
Pancreatic Β Cells ◽  
Inos Gene ◽  
Ifn Γ ◽  
Anti Inflammatory ◽  
Inos Gene Expression

Peroxisome proliferator-activated receptor (PPAR)γ agonists, such as 15-deoxy-Δ12,14-prostaglandin J2 (PGJ2) and troglitazone, have been shown to elicit anti-inflammatory effects in pancreatic β-cells that include inhibition of cytokine-stimulated inducible nitric oxide synthase (iNOS) gene expression and production of nitric oxide. In addition, these ligands impair IL-1-induced NF-κB and MAPK as well as IFN-γ-stimulated signal transducer and activator of transcription (STAT)1 activation in β-cells. The purpose of this study was to determine if PPARγ activation participates in the anti-inflammatory actions of PGJ2 in β-cells. Pretreatment of RINm5F cells for 6 h with PGJ2 results in inhibition of IL-1-stimulated IκB degradation and IFN-γ-stimulated STAT1 phosphorylation. Overexpression of a dominant-negative (dn) PPARγ mutant or treatment with the PPARγ antagonist GW-9662 does not modulate the inhibitory actions of PGJ2 on cytokine signaling in RINm5F cells. Although these agents fail to attenuate the inhibitory actions of PGJ2 on cytokine signaling, they do inhibit PGJ2-stimulated PPARγ response element reporter activity. Consistent with the inability to attenuate the inhibitory actions of PGJ2 on cytokine signaling, neither dnPPARγ nor GW-9662 prevents the inhibitory actions of PGJ2 on IL-1-stimulated iNOS gene expression or nitric oxide production by RINm5F cells. These findings support a PPARγ-independent mechanism by which PPARγ ligands impair cytokine signaling and iNOS expression by islets.

scholarly journals Increased colonic iNOS gene expression from sustained Western‐style diet exposure

2010 ◽  
Vol 24 (S1) ◽  
Author(s):  
Ella M Zimmerly ◽  
Hyeran Jang ◽  
Julia Sauer ◽  
Sang‐Woon Choi
Keyword(s):  
Gene Expression ◽  
Inos Gene ◽  
Diet Exposure ◽  
Inos Gene Expression

scholarly journals Effects of Lycopene, Indole-3-Carbinol, and Luteolin on Nitric Oxide Production and iNOS Expression are Organ-Specific in Rats

2010 ◽  
Vol 61 (3) ◽  
pp. 275-285 ◽  
Author(s):  
Evita Rostoka ◽  
Sergejs Isajevs ◽  
Larisa Baumane ◽  
Aija Line ◽  
Karina Silina ◽  
...  
Keyword(s):  
Gene Expression ◽  
Brain Cortex ◽  
Natural Compounds ◽  
Inos Expression ◽  
No Production ◽  
Nitric Oxide Production ◽  
Inos Gene ◽  
Organ Specific ◽  
The Brain ◽  
Inos Gene Expression

Effects of Lycopene, Indole-3-Carbinol, and Luteolin on Nitric Oxide Production and iNOS Expression are Organ-Specific in RatsNatural compounds are known to modify NO content in tissues; however, the biological activity of polyphenol-rich food often does not correspond to the effects of individual polyphenols on NO synthase activity. The aim of this study was to see how natural compounds luteolin, indole-3-carbinol, and lycopene modify NO production in rat tissues and change the expression of the iNOS gene and protein. Indole-3-carbinol produced multiple effects on the NO level; it significantly decreased NO concentration in blood, lungs, and skeletal muscles and increased it in the liver. Indole-3-carbinol enhanced lipopolyssaccharide (LPS)-induced NO production in all rat organs. It decreased iNOS gene expression in the brain cortex of animals that did not receive LPS and up-regulated it in the LPS-treated animals. Lycopene increased the iNOS gene transcription rate in the brain cortex of LPS-treated animals. Luteolin did not modify NO production in any organ of LPS-untreated rats, nor did it affect gene expression in the liver. In the brain it slightly decreased iNOS gene expression. Luteolin decreased NO production in the blood of LPS-treated animals and the number of iNOS-positive cells in these animals. Our results suggest that changes in tissue NO levels caused by natural compounds cannot be predicted from their effect on NOS expression or activity obtained in model systems. This stresses the importance of direct measurements of NO and NOS expression in animal tissues.

Inhibitory effect of recombinant iNOS gene expression on vasomotor function of canine basilar artery

2002 ◽  
Vol 283 (6) ◽  
pp. H2560-H2566 ◽  
Author(s):  
Daihiko Eguchi ◽  
Livius V. d'Uscio ◽  
Chris Wambi ◽  
Deborah Weiler ◽  
Imre Kovesdi ◽  
...  
Keyword(s):  
Gene Expression ◽  
Vascular Reactivity ◽  
Isometric Force ◽  
Cerebral Arteries ◽  
Vasomotor Function ◽  
Text Production ◽  
Inos Gene ◽  
Basilar Arteries ◽  
Endothelium Dependent Relaxation ◽  
Inos Gene Expression

The present study was designed to determine the effect of recombinant inducible nitric oxide (NO) synthase (iNOS) gene expression on vasomotor function in cerebral arteries. Isolated canine basilar arteries were exposed ex vivo (30 min at 37°C) to an adenoviral vector [107, 108, or 109plaque-forming units (pfu)/ml] encoding either the iNOS gene or the β-galactosidase reporter gene. Twenty-four hours after transduction, Western blot analysis demonstrated expression of iNOS protein only in iNOS (109pfu/ml)-transduced arteries. Immunohistochemical analysis localized iNOS expression predominantly in adventitia. Vascular reactivity of isolated basilar arteries was studied by isometric force recording. Concentration-response curves to UTP (10−9–10−3M) and diethylaminodiazen-1-ium-1,2-dioate (10−10–10−5M) were significantly shifted to the right in iNOS gene (109pfu/ml)-transduced rings compared with control and β-galactosidase-transduced rings ( P < 0.05, n = 5–6). Endothelium-dependent relaxation to bradykinin was significantly attenuated in iNOS-transduced rings ( P < 0.001, n = 8). The basal level of cGMP and superoxide anion (O[Formula: see text]·) production were elevated in iNOS-transduced rings ( P < 0.05, n = 7 for cGMP; P < 0.01, n = 6–9 for O[Formula: see text]· production). Our results suggest that expression of recombinant iNOS in cerebral arteries reduces vasomotor reactivity to both vasoconstrictor and vasodilator agonists. Attenuation of contractions is most likely due to functional antagonism between UTP and cGMP. Reduction of endothelium-dependent relaxation to bradykinin appears to be mediated in part by reduced reactivity of smooth muscle cells to NO.

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