scholarly journals Granulocyte–macrophage colony‐stimulating factor activates the transcription of nuclear factor kappa B and induces the expression of nitric oxide synthase in a skin dendritic cell line

2001 ◽  
Vol 79 (6) ◽  
pp. 590-596 ◽  
Author(s):  
M Teresa Cruz ◽  
Carlos B Duarte ◽  
Margarida Gonçalo ◽  
Américo Figueiredo ◽  
Arsélio P Carvalho ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Dendritic Cell ◽  
Nitric Oxide Synthase ◽  
Nuclear Factor Kappa B ◽  
Nuclear Factor ◽  
Colony Stimulating Factor ◽  
Macrophage Colony Stimulating Factor ◽  
Macrophage Colony ◽  
Oxide Synthase ◽  
Stimulating Factor

scholarly journals Enhanced production of nitric oxide by bone marrow cells and increased sensitivity to macrophage colony-stimulating factor (CSF) and granulocyte-macrophage CSF after benzene treatment of mice

Blood ◽  
1994 ◽  
Vol 83 (11) ◽  
pp. 3255-3263
Author(s):  
CJ Punjabi ◽  
JD Laskin ◽  
SM Hwang ◽  
L MacEachern ◽  
DL Laskin
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Nitric Oxide Production ◽  
Colony Stimulating Factor ◽  
Gm Csf ◽  
Oxide Production ◽  
Macrophage Colony Stimulating Factor ◽  
Macrophage Colony ◽  
Oxide Synthase ◽  
Stimulating Factor

Nitric oxide is a short-lived reactive mediator that inhibits bone marrow (BM) cell proliferation induced by granulocyte-macrophage colony- stimulating factor (GM-CSF). The present studies show that nitric oxide also inhibits macrophage colony-stimulating factor (M-CSF)-induced growth of mouse BM cells, an effect that was dependent on the presence of an inflammatory mediator and blocked by the nitric oxide synthase inhibitor, NG-monomethyl-L-arginine (L-NMA). Treatment of mice with the hematotoxicant benzene (800 mg/kg, intraperitoneally, two times per day, for 2 days) resulted in a significant increase in nitric oxide production by BM cells stimulated with lipopolysaccharide (LPS) and interferon gamma alone or in combination with M-CSF or GM-CSF. Cells from benzene-treated mice also displayed increased sensitivity to the growth-promoting effects of M-CSF and GM-CSF. These results suggest that benzene treatment of mice primes BM cells to inducers of nitric oxide. Northern blot analysis showed that this was, at least in part, caused by increased expression of mRNA for inducible nitric oxide synthase (iNOS). Surprisingly, treatment of mice with L-NMA was found to cause a depression in BM cell proliferation and to potentiate benzene-induced decreases in BM cellularity and increases in nitric oxide production. L-NMA administration also augmented nitric oxide production by BM cells. These data indicate that L-NMA is hematotoxic and suggest that it may have actions distinct from inhibition of nitric oxide synthase in the BM.

scholarly journals Enhanced production of nitric oxide by bone marrow cells and increased sensitivity to macrophage colony-stimulating factor (CSF) and granulocyte-macrophage CSF after benzene treatment of mice

Blood ◽  
1994 ◽  
Vol 83 (11) ◽  
pp. 3255-3263 ◽  
Author(s):  
CJ Punjabi ◽  
JD Laskin ◽  
SM Hwang ◽  
L MacEachern ◽  
DL Laskin
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Nitric Oxide Production ◽  
Colony Stimulating Factor ◽  
Gm Csf ◽  
Oxide Production ◽  
Macrophage Colony Stimulating Factor ◽  
Macrophage Colony ◽  
Oxide Synthase ◽  
Stimulating Factor

Abstract Nitric oxide is a short-lived reactive mediator that inhibits bone marrow (BM) cell proliferation induced by granulocyte-macrophage colony- stimulating factor (GM-CSF). The present studies show that nitric oxide also inhibits macrophage colony-stimulating factor (M-CSF)-induced growth of mouse BM cells, an effect that was dependent on the presence of an inflammatory mediator and blocked by the nitric oxide synthase inhibitor, NG-monomethyl-L-arginine (L-NMA). Treatment of mice with the hematotoxicant benzene (800 mg/kg, intraperitoneally, two times per day, for 2 days) resulted in a significant increase in nitric oxide production by BM cells stimulated with lipopolysaccharide (LPS) and interferon gamma alone or in combination with M-CSF or GM-CSF. Cells from benzene-treated mice also displayed increased sensitivity to the growth-promoting effects of M-CSF and GM-CSF. These results suggest that benzene treatment of mice primes BM cells to inducers of nitric oxide. Northern blot analysis showed that this was, at least in part, caused by increased expression of mRNA for inducible nitric oxide synthase (iNOS). Surprisingly, treatment of mice with L-NMA was found to cause a depression in BM cell proliferation and to potentiate benzene-induced decreases in BM cellularity and increases in nitric oxide production. L-NMA administration also augmented nitric oxide production by BM cells. These data indicate that L-NMA is hematotoxic and suggest that it may have actions distinct from inhibition of nitric oxide synthase in the BM.

scholarly journals Dexamethasone prevents granulocyte-macrophage colony-stimulating factor-induced nuclear factor-κB activation, inducible nitric oxide synthase expression and nitric oxide production in a skin dendritic cell line

2003 ◽  
Vol 12 (2) ◽  
pp. 71-78 ◽  
Author(s):  
Ana Luísa Vital ◽  
Margarida Gonçalo ◽  
M. Teresa Cruz ◽  
Américo Figueiredo ◽  
Carlos B. Duarte ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
No Production ◽  
Nuclear Factor ◽  
Colony Stimulating Factor ◽  
Gm Csf ◽  
Protein Levels ◽  
Macrophage Colony Stimulating Factor ◽  
Macrophage Colony ◽  
Oxide Synthase ◽  
Stimulating Factor

Aims:Nitric oxide (NO) has been increasingly implicated in inflammatory skin diseases, namely in allergic contact dermatitis. In this work, we investigated the effect of dexamethasone on NO production induced by the epidermal cytokine granulocyte-macrophage colony-stimulating factor (GM-CSF) in a mouse fetal skin dendritic cell line.Methods:NO production was assessed by the method of Griess. Expression of the inducible isoform of nitric oxide synthase (iNOS) protein was evaluated by western blot analysis and immunofluorescence microscopy. Western blot analysis was also performed to evaluate cytosolic IkappaB-alpha (IκB-α) protein levels. The electrophoretic mobility shift assay was used to evaluate the activation or inhibition of nuclear factor kappa B (NF-κB).Results:GM-CSF induced iNOS expression and NO production, and activated the transcription factor NF-κB. Dexamethasone inhibited, in a dose-dependent manner, NO production induced by GM-CSF. Addition of dexamethasone to the culture, 30 min before GM-CSF stimulation, significantly inhibited the cellular expression of iNOS. Dexamethasone also inhibited GM-CSF-induced NF-κB activation by preventing a significant decrease on the IκB-α protein levels, thus blocking NF-κB migration to the nucleus.Conclusions:The corticosteroid dexamethasone inhibits GM-CSF-induced NF-κB activation, iNOS protein expression and NO production. These results suggest that dexamethasone is a potent inhibitor of intracellular events that are involved on NO synthesis, in skin dendritic cells.

scholarly journals Efficiency of Estrogen Replacement Therapy in Osteoporosis

2018 ◽  
Vol 3 (3) ◽  
pp. 134
Author(s):  
Syed Mohammad Mazhar Uddin ◽  
Aatera Haq ◽  
Haris Sheikh ◽  
Uzair Yaqoob ◽  
Bushra Zafar Sayeed
Keyword(s):  
Nuclear Factor Kappa B ◽  
Calcium Absorption ◽  
Estrogen Therapy ◽  
Nuclear Factor ◽  
Colony Stimulating Factor ◽  
Nuclear Factor Kappa ◽  
Receptor Activator ◽  
Macrophage Colony Stimulating Factor ◽  
Macrophage Colony ◽  
Stimulating Factor

Estrogen therapy has been taken as a settled approach for both prevention and treatment of osteoporosis, especially in post-menopausal women as well as for the treatment of symptoms associated with menopause. Recent studies suggest that nuclear factor kappa-B ligand/receptor activator of nuclear factor kappa-B/osteoprotegerin system plays a signi cant role in osteoclastic activity regulation, with receptor activator of nuclear factor kappa-B ligand signaling in the presence of macrophage colony stimulating factor leading to increase in osteoclastic differentiation and functioning while osteoprotegerin neutralizing receptor activator of nuclear factor kappa-B ligand. Estrogen acts by increasing osteoprotegerin levels, and decreasing macrophage colony stimulating factor and receptor activator of nuclear factor kappa-B, thereby reducing bone resorption. Furthermore, estrogen is also known to be causing increased calcium absorption through gut and kidneys. The use of estrogen therapy in patients of osteoporosis is also considered to be highly cost effective. On the negative side, studies have shown that oral estrogen therapy can lead to complications like cholelithiasis, thrombophlebitis and pulmonary embolism, the most detrimental being endometrial cancer. But studies have shown that it can be virtually eliminated with the addition of progesterone in the cyclic combined regimen. Majority of bene cial effects occur with long term use of estrogen therapy, but the compliance by most of women appears to be poor and is usually due to lack of awareness, misconceptions, advice of physician and phobia of side effects. Additional studies should therefore be conducted to evaluate in detail the causes of non-compliance and strategies to improve compliance. The bene t of quality of life improvement with estrogen therapy should be taken into account and further evaluated via studies.

scholarly journals Isolation and characterization of cytotoxic and anti-inflammatory constituents from Scoparia dulcis L

2020 ◽  
Vol 44 (7-8) ◽  
pp. 381-387
Author(s):  
Mohammad Nur-e-Alam ◽  
Sarfaraz Ahmed ◽  
Muhammad Yousaf ◽  
Shabana I Khan ◽  
Ramzi A Mothana ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Acetic Acid ◽  
Nitric Oxide Synthase ◽  
Inducible Nitric Oxide Synthase ◽  
Nuclear Factor Kappa B ◽  
Nuclear Factor ◽  
Scoparia Dulcis ◽  
Anti Inflammatory ◽  
Oxide Synthase ◽  
Inducible Nitric Oxide

Scoparia dulcis L. is one of the edible widely distributed Scropholariaceae species in Asia, Africa and America. It is used in the treatment of respiratory and inflammatory diseases, diabetes, hypertension, cancer, hepatitis and tuberculosis. A phytochemical investigation on S. dulcis led to the isolation of two new acyclic diterpenes Acetic acid 6-hydroxy-2-(6-hydroxy-4-methyl-hex-4-enylidene)-4,8-dimethyl-undeca-4,8-dienyl ester (1) and Acetic acid 8-hydroxy-2-(6-hydroxy-4-methyl-hex-4-enylidene)-6,10-dimethyl-undeca-5,9-dienyl ester (2) in addition to eight known compounds (3–10), namely scopadulciol (3), 4- epi-scopadulcic acid B (4), dulcidiol (5), scopadulcic acid B (6), hymenoxin (7), glutinol (8), eupatilin (9) and 5-demethylnobiletin (10). The structures elucidation was performed using spectroscopic means, including 1D and 2D nuclear magnetic resonance and high-resolution electrospray ionization mass spectrum spectrometric analysis. Furthermore, the isolated compounds were investigated for their anti-inflammatory activity through the determination of inhibition of nuclear factor-kappa B activity in human chondrosarcoma (SW1353) cells, the inhibition of inducible nitric oxide synthase mouse macrophages (RAW264.7) and the decrease in cellular oxidative stress in HepG2 cells. Moreover, the cytotoxic activity was investigated against four cancer and two kidney cell lines. Among the isolates, 3, 5 and 10 showed anti-inflammatory activity in terms of inhibiting nuclear factor-kappa B and inducible nitric oxide synthase. Compounds 3–5 were the most cytotoxic towards cancer cell lines (IC50: 3.8 µM to 42.3 µM) followed by 10 (IC50: 30.9- > 64.4 µM). Cytotoxicity of compounds 3–5 was comparable to the activity of doxorubicin.

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