On the Mode of Action and Biochemical Properties of Anti-Inflammatory Drugs*

1979 ◽  
Vol 7 (4) ◽  
pp. 655-657 ◽  
Author(s):  
SHEIKH A. SAEED ◽  
PATRICIA A. KENDALL ◽  
NAEEM M. BUTT ◽  
HARRY O. J. COLLIER
Keyword(s):  
Mode Of Action ◽  
Biochemical Properties ◽  
Inflammatory Drugs ◽  
Anti Inflammatory

scholarly journals New Perspectives on Aspirin and the Endogenous Control of Acute Inflammatory Resolution

2006 ◽  
Vol 6 ◽  
pp. 1048-1065 ◽  
Author(s):  
Thea Morris ◽  
Melanie Stables ◽  
Derek W. Gilroy
Keyword(s):  
Mode Of Action ◽  
Acute Inflammation ◽  
Lipid Mediators ◽  
The Other ◽  
Endogenous Control ◽  
Protective Properties ◽  
Traditional Mode ◽  
Inflammatory Drugs ◽  
Cox 2 ◽  
Anti Inflammatory

Aspirin is unique among the nonsteroidal anti-inflammatory drugs in that it has both anti-inflammatory as well as cardio-protective properties. The cardio-protective properties arise form its judicious inhibition of platelet-derived thromboxane A2over prostacyclin, while its anti-inflammatory effects of aspirin stem from its well-established inhibition of prostaglandin (PG) synthesis within inflamed tissues. Thus aspirin and the other NSAIDs have popularised the notion of inhibiting PG biosynthesis as a common anti-inflammatory strategy based on the erroneous premise that all eicosanoids are generally detrimental to inflammation. However, our fascination with aspirin has shown a more affable side to lipid mediators based on our increasing interest in the endogenous control of acute inflammation and in factors that mediate its resolution. Epi-lipoxins (epi-LXs), for instance, are produced from aspirin’s acetylation of inducible cyclooxygenase 2 (COX-2) and together with Resolvins represent an increasingly important family of immuno-regulatory and potentially cardio-protective lipid mediators. Aspirin is beginning to teach us what nature knew all along – that not all lipid mediators are bad. It seems that while some eicosanoids are pathogenic in a variety of diseases, others are unarguable protective. In this review we will re-count aspirin’s colorful history, discuss its traditional mode of action and the controversies associated therewith, as well as highlight some of the new pathways in inflammation and the cardiovascular systems that aspirin has recently revealed.

Possible Differences In The Mode Of Action Of Ditazole And Non-Steroidal Anti-Inflammatory Drugs As Potential Antithrombotic Agents

1981 ◽  
Author(s):  
A K Sim ◽  
A P McCraw ◽  
L Caprino ◽  
F Antonetti ◽  
L Morelli
Keyword(s):  
Platelet Aggregation ◽  
Mode Of Action ◽  
Platelet Rich Plasma ◽  
Shape Change ◽  
Dose Range ◽  
Oral Drug ◽  
Inflammatory Drugs ◽  
Anti Inflammatory ◽  
Induced Aggregation ◽  
Platelet Shape

Ditazole (4,5-diphenyl-2-diethanolamino-oxazole), a weak anti-inflammatory drug, has been shown to be a potent inhibitor of platelet aggregation, adhesiveness and bleeding time. Acetylsalicylic acid (ASA), dipyridamole and a combination of these two drugs induced a platelet shape change which was much shorter lasting than their effect on platelet aggregation. Conversely, similar doses of ditazole induced a potent shape change but no effect on aggregation. Ditazole has now been shown to reversibly antagonise thromboxane A2 (TXA2)-induced contraction of rabbit aortic strips at an optimal concentration of 25 μm in the perfusate. Separately, over a dose range of 50-400 mg/kg/p.o., TXA2 production was inhibited between 39% and 85% in spontaneously clotted rabbit blood. In addition, we have shown that TXA2 formation following arachidonic acid-induced aggregation of platelet-rich plasma (PRP) is similarly inhibited. Ditazole however did not inhibit prostacyclin (PGI2) production in rabbit aortic rings following oral drug administration over a dose range of 50-400 mg/kg. At 1000 and 2000 mg/kg PGI2 production was inhibited by 23% and 41% respectively. TXA2 and PGI2 levels were measured by radioimmunoassay of their stable derivatives TXB2 and 6-keto-PGF1α. It is suggested that the mode of action of ditazole may be more specific than the cyclo-oxygenase/PG-synthetase blocking activity of most other non-steroidal anti-inflammatory drugs.

Biochemical properties of anti-inflammatory drugs—II

1964 ◽  
Vol 13 (3) ◽  
pp. 413-420 ◽  
Author(s):  
H. Boström ◽  
K. Berntsen ◽  
M.W. Whitehouse
Keyword(s):  
Biochemical Properties ◽  
Inflammatory Drugs ◽  
Anti Inflammatory

Biochemical properties of anti-inflammatory drugs—XII

1971 ◽  
Vol 20 (12) ◽  
pp. 3309-3320 ◽  
Author(s):  
M.W. Whitehouse ◽  
I. Kippen ◽  
J.R. Klinenberg
Keyword(s):  
Biochemical Properties ◽  
Inflammatory Drugs ◽  
Anti Inflammatory
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