Anti-inflammatory effects of the butanolic fraction of Byrsonima verbascifolia leaves: Mechanisms involving inhibition of tumor necrosis factor alpha, prostaglandin E2 production and migration of polymorphonuclear leucocyte in vivo experimentation

2016 ◽  
Vol 31 ◽  
pp. 123-131 ◽  
Author(s):  
Aline Aparecida Saldanha ◽  
João Máximo de Siqueira ◽  
Ana Hortência Fonsêca Castro ◽  
Rosy Iara Maciel de Azambuja Ribeiro ◽  
Flávio Martins de Oliveira ◽  
...  
Keyword(s):  
Tumor Necrosis Factor ◽  
Prostaglandin E2 ◽  
Tumor Necrosis Factor Alpha ◽  
Tumor Necrosis ◽  
Polymorphonuclear Leucocyte ◽  
Necrosis Factor Alpha ◽  
Factor Alpha ◽  
And Migration ◽  
Necrosis Factor

Low-dose prostacyclin has potent capillary permeability-reducing effect in cat skeletal muscle in vivo

1997 ◽  
Vol 273 (1) ◽  
pp. H200-H207 ◽  
Author(s):  
A. D. Moller ◽  
P. O. Grande
Keyword(s):  
Tumor Necrosis Factor ◽  
Tumor Necrosis Factor Alpha ◽  
Tumor Necrosis ◽  
Vascular Tone ◽  
Low Dose ◽  
Capillary Permeability ◽  
Necrosis Factor Alpha ◽  
Factor Alpha ◽  
Necrosis Factor

The dose-response effects of intravenous infusion of prostacyclin on capillary permeability (the capillary filtration coefficient technique), hydrostatic capillary pressure, transcapillary filtration, and vascular tone were analyzed in vivo on cat skeletal muscle from a normal and an increased permeability level. Increased permeability was accomplished by intra-arterial infusion of tumor necrosis factor-alpha or histamine. Permeability effects of bradykinin were also analyzed. Prostacyclin decreased capillary permeability by 8% at a dose of 0.1 ng.kg-1.min-1 and at most by 30% below control attained at 2 ng.kg-1.min-1, also with no effect on vascular tone and hydrostatic capillary pressure. The permeability increase by tumor necrosis factor-alpha and histamine (by 54 and 73%) was more than counteracted by the simultaneous infusion of prostacyclin at 2 ng.kg-1.min-1. The vasodilator effect of tumor necrosis factor-alpha was also restituted. Indomethacin (prostacyclin inhibitor)-induced increase in capillary permeability (25%) was more than restituted by prostacyclin at 2 ng.kg-1.min-1. Surprisingly, bradykinin decreased capillary permeability. We conclude that endogenous prostacyclin may be a physiological regulator of capillary permeability and that low-dose prostacyclin infusion may have clinical relevance in states of increased permeability.

scholarly journals Leptin Mediates In Vivo Neutrophil Migration: Involvement of Tumor Necrosis Factor-Alpha and CXCL1

2018 ◽  
Vol 9 ◽  
Author(s):  
Glaucia Souza-Almeida ◽  
Heloisa D’Avila ◽  
Patricia E. Almeida ◽  
Tatiana Luna-Gomes ◽  
Sally Liechocki ◽  
...  
Keyword(s):  
Tumor Necrosis Factor ◽  
Tumor Necrosis Factor Alpha ◽  
Tumor Necrosis ◽  
Neutrophil Migration ◽  
Necrosis Factor Alpha ◽  
Factor Alpha ◽  
Necrosis Factor

scholarly journals Thalidomide selectively inhibits tumor necrosis factor alpha production by stimulated human monocytes.

1991 ◽  
Vol 173 (3) ◽  
pp. 699-703 ◽  
Author(s):  
E P Sampaio ◽  
E N Sarno ◽  
R Galilly ◽  
Z A Cohn ◽  
G Kaplan
Keyword(s):  
Tumor Necrosis Factor ◽  
Tumor Necrosis Factor Alpha ◽  
Tumor Necrosis ◽  
Interleukin 1 ◽  
Human Monocyte ◽  
Tnf Alpha ◽  
Necrosis Factor Alpha ◽  
Factor Alpha ◽  
Necrosis Factor

Thalidomide selectively inhibits the production of human monocyte tumor necrosis factor alpha (TNF-alpha) when these cells are triggered with lipopolysaccharide and other agonists in culture. 40% inhibition occurs at the clinically achievable dose of the drug of 1 micrograms/ml. In contrast, the amount of total protein and individual proteins labeled with [35S]methionine and expressed on SDS-PAGE are not influenced. The amounts of interleukin 1 beta (IL-1 beta), IL-6, and granulocyte/macrophage colony-stimulating factor produced by monocytes remain unaltered. The selectivity of this drug may be useful in determining the role of TNF-alpha in vivo and modulating its toxic effects in a clinical setting.

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