Compounds > 13-hydroxy-9-11-octadecadienoic-acid

13-hydroxy-9-11-octadecadienoic-acid and Shock--Septic

13-hydroxy-9-11-octadecadienoic-acid has been researched along with Shock--Septic* in 1 studies

Other Studies

1 other study(ies) available for 13-hydroxy-9-11-octadecadienoic-acid and Shock--Septic

Article	Year
Lipoxygenase inhibitors but not site specific 5-lipoxygenase blockers protect against endotoxic shock and inhibit production of tumor necrosis factor. Eicosanoids, 1992, Volume: 5 Suppl In the present study it was found that lipoxygenase inhibitors prevent LPS-, but not tumor necrosis factor alpha (TNF alpha)-evoked lethality. The specific 5-lipoxygenase inhibitors (MK-886, CGS-8515) were uneffective in endotoxin-induced shock. The 5-lipoxygenase inhibitors interfered with LTC4 formation in macrophages while they did not affect endotoxin induced TNF alpha-formation, neither in cell cultures nor in mice. The potency of other, less specific lipoxygenase blockers to suppress TNF alpha formation correlated quantitatively with their ability to interfere with 13-HODD synthesis. Based on the fact that a tight correlation exists between inhibition of TNF alpha synthesis and 13-HODD formation, this product might be important for TNF alpha formation. Topics: Animals; Cell Line; Linoleic Acids; Lipopolysaccharides; Lipoxygenase Inhibitors; Macrophages; Mice; Shock, Septic; SRS-A; Tumor Necrosis Factor-alpha	1992

Article

Year

Lipoxygenase inhibitors but not site specific 5-lipoxygenase blockers protect against endotoxic shock and inhibit production of tumor necrosis factor.

Eicosanoids, 1992, Volume: 5 Suppl

In the present study it was found that lipoxygenase inhibitors prevent LPS-, but not tumor necrosis factor alpha (TNF alpha)-evoked lethality. The specific 5-lipoxygenase inhibitors (MK-886, CGS-8515) were uneffective in endotoxin-induced shock. The 5-lipoxygenase inhibitors interfered with LTC4 formation in macrophages while they did not affect endotoxin induced TNF alpha-formation, neither in cell cultures nor in mice. The potency of other, less specific lipoxygenase blockers to suppress TNF alpha formation correlated quantitatively with their ability to interfere with 13-HODD synthesis. Based on the fact that a tight correlation exists between inhibition of TNF alpha synthesis and 13-HODD formation, this product might be important for TNF alpha formation.

Topics: Animals; Cell Line; Linoleic Acids; Lipopolysaccharides; Lipoxygenase Inhibitors; Macrophages; Mice; Shock, Septic; SRS-A; Tumor Necrosis Factor-alpha

1992