ChemInform Abstract: Synthesis and Conformation of 2-((3-(1-Hydroxyhexyl)phenoxy)methyl) quinoline (VI), a 5-Lipoxygenase Inhibitor and Leukotriene Antagonist.

ChemInform ◽  
2010 ◽  
Vol 24 (39) ◽  
pp. no-no
Author(s):  
J. D. WHITE ◽  
K. M. YAGER ◽  
F. STAPPENBECK
Keyword(s):  
Lipoxygenase Inhibitor ◽  
Leukotriene Antagonist

Endogenous prostaglandins modulate histamine-induced contraction in canine tracheal smooth muscle

1985 ◽  
Vol 58 (3) ◽  
pp. 859-868 ◽  
Author(s):  
S. A. Shore ◽  
W. S. Powell ◽  
J. G. Martin
Keyword(s):  
Smooth Muscle ◽  
Nordihydroguaiaretic Acid ◽  
Isometric Tension ◽  
Tracheal Smooth Muscle ◽  
Lipoxygenase Inhibitor ◽  
Synthesis Inhibitor ◽  
Leukotriene Antagonist ◽  
Endogenous Prostaglandins ◽  
Histamine Response

We studied the role of endogenous prostaglandins in modulating the histamine response of canine tracheal smooth muscle (TSM) in vitro. Indomethacin (INDO) (10(-7) - 10(-5) M), a cyclooxygenase and prostaglandin synthesis inhibitor, significantly increased maximum histamine-induced tension (Tmax) and decreased the concentration of histamine required to produce 50% of Tmax (EC50). Acetylsalicylic acid (10(-5) -5 X 10(-4) M), another less potent cyclooxygenase inhibitor, also decreased EC50. Neither the lipoxygenase inhibitor nordihydroguaiaretic acid nor the leukotriene antagonist FPL 55712 had any effect on histamine-induced tension in INDO-pretreated TSM. INDO reduced the standard deviation of EC50 from 0.47 in control TSM (n = 51) to 0.26 in INDO-pretreated TSM (n = 31) (P less than 0.02). High-pressure liquid chromatography established prostacyclin (PGI2), through its degradation product 6-oxo-PGF1 alpha, as the predominant prostaglandin produced by canine TSM. Exogenous PGI2 caused a concentration-dependent relaxation of histamine-contracted TSM. In the tissue bath, spontaneous efflux of 6-oxo-PGF1 alpha from TSM, as measured by radioimmunoassay, averaged 4.7 ng . g muscle-1 . min-1 and increased to 10 ng/g muscle (n = 10, P less than 0.001) with administration of histamine. The isometric tension produced by histamine (10(-4) M) was inversely linearly correlated with the log concentration of endogenous 6-oxo-PGF1 alpha (r = 0.81, P less than 0.01). Our results are consistent with an important role for endogenous bronchodilating prostaglandins, probably prostacyclin, in determining both the histamine sensitivity of canine TSM in vitro and its variability among individual animals.

scholarly journals Immune complex induced arthritis in rats: role of lipid mediators on cell infiltration

1996 ◽  
Vol 5 (2) ◽  
pp. 104-109 ◽  
Author(s):  
F. A. C. Rocha ◽  
L. E. C. Andrade ◽  
S. Jancar
Keyword(s):  
Immune Complex ◽  
Platelet Activating Factor ◽  
Lipid Mediators ◽  
Cell Infiltration ◽  
Blue Dye ◽  
Histopathological Analysis ◽  
Lipoxygenase Inhibitor ◽  
Arthritis Model ◽  
Leukotriene Antagonist ◽  
Mediate Cell

We investigated the participation of lipid mediators in an experimental immune complex (IC) arthritis model in rats. The animals were subjected to intraarticular injection of anti-bovine sertLm albumin (BSA) IgG antibodies followed by i.v. injection of BSA. Histopathological analysis of the synovial membranes disclosed infiltration of polymorphonuclear (PMN) cells and vascular congestion. Slight increase in vascular permeability, measured by Evans blue dye extravasation into the joints, was detected after 3 h of arthritis. Cellular influx into the articular cavities was most evident at the sixth hour of arthritis with predominance of PMN. Pretreatment with either indomethacin, a cyclooxygenase inhibitor, or L-660,711, a peptido-leukotriene antagonist, did not inhibit cell infiltration, whereas pretreatment with either L-663,536, a 5-lipoxygenase inhibitor, or L-655,240, a thromboxane antagonist, significantly inhibited the phenomenon. Pretreatment with WEB 2170, a platelet activating factor (PAF) antagonist, also significantly inhibited cell influx. These results suggest that thromboxane, LTB4and PAF mediate cell infiltration in this IC arthritis model.

scholarly journals Effect of a 5-lipoxygenase inhibitor and leukotriene antagonist (PF 5901) on antigen-induced airway responses in neonatally immunized rabbits

1994 ◽  
Vol 112 (1) ◽  
pp. 292-298 ◽  
Author(s):  
Caroline M. Herd ◽  
Donna Donigi-Gale ◽  
T. Scott Shoupe ◽  
D.A. Burroughs ◽  
M. Yeadon ◽  
...  
Keyword(s):  
Lipoxygenase Inhibitor ◽  
Leukotriene Antagonist ◽  
Airway Responses

Platelet Aggregation in Whole Blood: The Role of Thromboxane A2 and Adenosine Diphosphate

1985 ◽  
Vol 54 (03) ◽  
pp. 612-616 ◽  
Author(s):  
A J Carter ◽  
S Heptinstall
Keyword(s):  
Platelet Aggregation ◽  
Whole Blood ◽  
Adenosine Diphosphate ◽  
Blood Platelet ◽  
Thromboxane B2 ◽  
Lipoxygenase Inhibitor ◽  
Thromboxane Synthase Inhibitor ◽  
Synthase Inhibitor

SummaryThe platelet aggregation that occurred in whole blood in response to several aggregating agents (collagen, arachidonic acid, adenosine diphosphate, adrenaline and thrombin) was measured using an Ultra-Flo 100 Whole Blood Platelet Counter. The amounts of thromboxane B2 produced were measured by radioimmunoassay. The effects of various inhibitors of thromboxane synthesis and the effects of apyrase, an enzyme that destroys adenosine diphosphate, were determined.Platelet aggregation was always accompanied by the production of thromboxane B2, and the amounts produced depended on the nature and concentration of the aggregating agent used. The various inhibitors of thromboxane synthesis - aspirin and flurbiprofen (cyclo-oxygenase inhibitors), BW755C (a cyclo-oxygenase and lipoxygenase inhibitor) and dazoxiben (a selective thromboxane synthase inhibitor) - did not markedly inhibit aggregation. Results obtained using apyrase showed that adenosine diphosphate contributed to the aggregation process, and that its role must be acknowledged when devising means of inhibiting platelet aggregation in vivo.

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