The effect of high concentration of glucose on the production of proinflammatory cytokines and nitric oxide induced by lipopolysaccharides from periodontopathic bacteria

2008 ◽  
Vol 38 (3) ◽  
pp. 511
Author(s):  
Sung-Jo Kim
Keyword(s):  
Nitric Oxide ◽  
Proinflammatory Cytokines ◽  
High Concentration ◽  
Periodontopathic Bacteria

Effect of nitric oxide on Sertoli cell microtubule of piglets

2009 ◽  
Vol 6 (3) ◽  
pp. 257-263 ◽  
Author(s):  
Yang Li ◽  
Wang Xian-zhong ◽  
Yang Meng-bo ◽  
Zhang Jia-hua
Keyword(s):  
Nitric Oxide ◽  
Enzyme Activity ◽  
Protein Kinase ◽  
Cell Viability ◽  
Sodium Nitroprusside ◽  
Sertoli Cell ◽  
Sertoli Cells ◽  
High Concentration ◽  
Treatment Results ◽  
Anti Oxidant

AbstractTo illustrate the effect of nitric oxide (NO) on the microtubules of Sertoli cells (SC), SCs of piglets were treated with sodium nitroprusside (SNP). Changes in cell viability, anti-oxidant activity, enzyme activity and p38 mutagen-activated protein kinase (p38MAPK) activation were detected. The results were as follows. A low concentration of NO can keep SC microtubule and cell viability normal, and a high concentration of NO could increase p38MAPK activation, decrease anti-oxidant activity and transferrin secretion, and destroy the structure and distribution of the microtubules. The results suggest that SNP treatment results in an increase in NO in SCs and decreased cell anti-oxidant activity. The high concentration of NO destroys cell microtubules by activating p38MAPK.

Rutin inhibits β-amyloid aggregation and cytotoxicity, attenuates oxidative stress, and decreases the production of nitric oxide and proinflammatory cytokines

2012 ◽  
Vol 33 (3) ◽  
pp. 482-490 ◽  
Author(s):  
Shao-wei Wang ◽  
Yu-Jiong Wang ◽  
Ya-jing Su ◽  
Wei-wei Zhou ◽  
Shi-gao Yang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Nitric Oxide ◽  
Proinflammatory Cytokines ◽  
Amyloid Aggregation ◽  
Β Amyloid

Effects of tiludronate and ibandronate on the secretion of proinflammatory cytokines and nitric oxide from macrophages in vitro

Life Sciences ◽  
1998 ◽  
Vol 62 (8) ◽  
pp. PL95-PL102 ◽  
Author(s):  
Jukka Mönkkönen ◽  
Johanna Similä ◽  
Michael J. Rogers
Keyword(s):  
Nitric Oxide ◽  
Proinflammatory Cytokines

Human placental and fetal membrane nitric oxide synthase activity before, during and after labour at term

1995 ◽  
Vol 7 (6) ◽  
pp. 1505 ◽  
Author(s):  
Iulio JL Di ◽  
NM Gude ◽  
RG King ◽  
SP Brennecke
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Caesarean Section ◽  
Normal Vaginal Delivery ◽  
Fetal Membrane ◽  
High Concentration ◽  
Experimental Conditions ◽  
Nos Inhibitor ◽  
Tissue Specimens ◽  
Oxide Synthase

The aim of this study was to determine whether any labour-associated changes in nitric oxide synthase (NOS) activity occur in human placenta and fetal membranes. NOS activity in amnion, choriodecidua, and placenta obtained from women before (at Caesarean section, not in labour), during (at Caesarean section, in labour) and after (spontaneous onset labour, normal vaginal delivery) labour was assessed by measuring conversion of radio-labelled L-arginine to L-citrulline. NOS activity, as judged by its inhibition by the specific NOS inhibitor N omega-nitro-L-arginine, was present in placental and amnionic tissues, but not in choriodecidual tissue specimens. Activity detected in choriodecidua was significantly blocked during incubation with a high concentration of valine, suggesting that L-arginine was being consumed by reactions other than NOS under the experimental conditions in that tissue. There were no significant differences among the labour groups in either amnion or placental NOS activities measured in the presence of 1 microM L-arginine. Amnion NOS activity was significantly less than that in placenta. Placental V(max) and Km values (determined after removal of endogenous L-arginine) did not differ significantly among the different labour groups.

In Situ Detection of Inflammatory Cytokines and Apoptosis in Pemphigus Foliaceus Patients

2009 ◽  
Vol 133 (1) ◽  
pp. 97-100
Author(s):  
Denise Bertulucci Rocha Rodrigues ◽  
Sanivia Aparecida Lima Pereira ◽  
Marlene Antônia dos Reis ◽  
Sheila Jorge Adad ◽  
João Eduardo Caixeta ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Inducible Nitric Oxide Synthase ◽  
Proinflammatory Cytokines ◽  
Interleukin 1 ◽  
Terminal Deoxynucleotidyl Transferase ◽  
Pemphigus Foliaceus ◽  
Endemic Pemphigus Foliaceus ◽  
Oxide Synthase ◽  
Inducible Nitric Oxide

Abstract Context.—Endemic pemphigus foliaceus, or fogo selvagem, is a chronic autoimmune disease characterized by the formation of intraepidermal blisters that reduce adhesion between keratinocytes. Endemic pemphigus foliaceus is associated with the presence of autoantibodies and high levels of cytokines involved in the inflammatory response. Objectives.—To evaluate the expression of the proinflammatory cytokines interleukin 1, interferon γ, and tumor necrosis factor α; the proapoptotic inducers Fas and inducible nitric oxide synthase; and the apoptosis inhibitor Bcl-2; and to evaluate the presence of apoptosis. Design.—Skin biopsies from 13 patients with endemic pemphigus foliaceus and controls were evaluated by immunohistochemistry and apoptosis was determined by terminal deoxynucleotidyl transferase–mediated dUTP nick-end labeling assay. Results.—Proinflammatory cytokines were only detected in cells of the inflammatory exudate. Inducible nitric oxide synthase, Fas, and Bcl-2 were expressed by both epithelial and inflammatory cells. Epithelial apoptosis was observed in 12 cases (92.3%), and subepithelial apoptosis in 11 cases (85%). Conclusions.—This study suggests that apoptosis as well as the local production of proinflammatory cytokines are associated with endemic pemphigus foliaceus lesions. These results may contribute to the development of new therapeutic approaches to endemic pemphigus foliaceus.

Proinflammatory cytokines depress cardiac efficiency by a nitric oxide-dependent mechanism

1998 ◽  
Vol 275 (3) ◽  
pp. H1016-H1023 ◽  
Author(s):  
Donna Panas ◽  
Fadi H. Khadour ◽  
Csaba Szabó ◽  
Richard Schulz
Keyword(s):  
Nitric Oxide ◽  
Proinflammatory Cytokines ◽  
Heart Function ◽  
Early Response ◽  
Interferon Γ ◽  
Cardiac Efficiency ◽  
Cardiac Work ◽  
Rat Hearts ◽  
Inos Inhibitor ◽  
Factor Α

Proinflammatory cytokines (interleukin-1β, tumor necrosis factor-α, and interferon-γ; Cytomix) depress myocardial contractile work partially by stimulating expression of inducible nitric oxide (NO) synthase (iNOS). Because NO and peroxynitrite inhibit myocardial O2 consumption (MV˙o 2), we examined whether this mechanism contributes to reduced cardiac work. In control isolated working rat hearts, cardiac work was stable for 60 min, followed by a decline from 60 to 120 min, without change in MV˙o 2. Cardiac efficiency (work/MV˙o 2) was therefore reduced from 60 to 120 min. Cytomix shortened the onset (within 20–40 min) and enhanced the depression in cardiac work and efficiency and inhibited MV˙o 2 after 80 min. Mercaptoethylguanidine (MEG), an iNOS inhibitor and peroxynitrite scavenger, or the glucocorticoid dexamethasone (Dex) abolished the effects of Cytomix. iNOS expression was increased 10-fold by Cytomix and abolished by Dex but not MEG. That cytokine-induced depression in cardiac work precedes the reduction in MV˙o 2 suggests, at least in the early response, that NO and/or peroxynitrite may not impair heart function by inhibiting mitochondrial respiration but reduce the heart’s ability to utilize ATP for contractile work.

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