Vane,Effects of Anti-Inflammatory Drugs on ..

EUROLAC is Ketorolac trometamol, a potent analgesic agent of non-steroidal, anti-inflammatory class (NSAID). Its mode of action is to inhibit the cyclo-oxygenase enzyme system and hence prostaglandin synthesis, and it demonstrates a minimal anti-inflammatory effect at its analgesic dose. Eurolac is not an anesthetic agent and possesses no sedative or anxiolytic properties; therefore it is not recommended as a pre-operative medication for the support of anesthesia when these effects are required. It is not an opioid and has no known effects on opioid receptors. Indicated for the short-term management of postoperative pain.

Inhibition of Prostaglandin Biosynthesis by Anti-Inflammatory ..

Effects of anti-inflammatory drugs on ..

Effects on antiinflammatory drugs on prostaglandin biosynthesis

Nonsteroidal anti-inflammatory drugs (NSAIDs) are among the most commonly used drugs in the world for the treatment of osteoarthritis (OA) symptoms, and are taken by 20-30% of elderly people in developed countries. Because of the potential for significant side effects of these medications on the liver, stomach, gastrointestinal tract and heart, including death, treatment guidelines advise against their long term use to treat OA. One of the best documented but lesser known long-term side effects of NSAIDs is their negative impact on articular cartilage.

Effects of anti-inflammatory drugs on prostaglandin ..

The suggestion that indomethacin accelerates the bone destruction in osteoarthritis of the hip was first made by Coke in 1967;103 subsequent reports have been numerous that provide further clinical evidence of the damaging effects of non-steroidal anti-inflammatory drugs on osteoarthritic hips.104-107 In one retrospective investigation of the relationship between the use of non-steroidal anti-inflammatory drugs on hip destruction in primary osteoarthritis of the hip, 70 hips were studied in 64 patients. Cranial acetabular migration, a measure of acetabular destruction, was present in 37 hips and absent in 33. Regular intake of NSAIDs was noted for 31 of the 37 migrating hips. In regard to the other six, three took NSAIDs on and off and only three of the 37 did not take NSAIDs. Those patients with serious hip destruction when compared with those who did not have the acetabular destruction did not differ in sex, age, pain grading, or walking ability. The only significant difference was the amount of NSAIDs taken. According to the researchers, NSAID use was associated with progressive formation of multiple small acetabular and femoral subcortical cysts and subchondral bone thinning. They concluded, “The association of acetabular bone destruction with regular NSAID intake in patients with osteoarthritis of the hip adds further evidence to the clinical and experimental observations on the powerful and potentially harmful effects of these drugs on cartilage and bone.”108 In this study the NSAIDs used regularly and associated with acetabular migration in this series were indomethacin (14 hips); ibuprofen (8 hips); naproxen (3 hips); sulindac, aspirin, and piroxicam (2 hips each); flurbiprofen, azapropazone, diclofenac, fenclofenac, and ketoprofen (1 hip each). The authors noted, “This study suggests caution in the widespread use of NSAIDs for osteoarthritis of the hip…”

Effects of kinesiotaping versus non-steroidal anti-inflammatory drugs ..
Effects of kinesiotaping versus non-steroidal anti-inflammatory drugs and ..

Pharmacology & Pharmaceutical Medicine

To determine the reliability of the co-culturemodel, the model was validated using anti-atherosclerotic agent,atorvastatin, which has known lipid-lowering and anti-inflammatoryeffects, and the non-steroidal anti-inflammatory drug,indomethacin. The experimental results demonstrated that treatmentwith atorvastatin resulted in an effective reduction of theEC-surface adhered cell count and inhibition of the expression ofconnexin-43 (), decreasedlevels of TNF-α and MCP-1 in the EC supernatant () and MMP-2, IL-6, and MDA in SMCsupernatant (), anddownregulation of the mRNA expression of NF-κB and upregulation ofthe mRNA expression of PPARγ in the ECs (). By contrast, indomethacinreduced the EC surface-adhered cell count, inhibited the secretionof TNF-α and MCP-1 by the ECs, and suppressed the mRNA expressionof NF-κB. However, treatment with indomethacin revealed nosignificant effects on the other indices. These results suggestedthat this model effectively reflected the efficacy ofanti-athero-sclerotic agents with an anti-inflammatory effect, andmay be used to identify drugs with potential anti-inflammatory andanti-atherosclerotic activities, and to assess their efficacy.

Biosynthesis of prostaglandin E 2 in human skin: subcellular localization and inhibition by unsaturated fatty acids and anti-inflammatory drugs

The Anti-Inflammatory Effects of Prostaglandins | JIM

Atherosclerosis is commonly understood as aninflammatory vascular disease, and targeting key inflammatorymediators through the inhibition of cytokine activities is asuccessful approach for preventing or slowing the progression ofatherosclerosis (). Previousstudies have started to use inflammatory cytokines directly, asinflammatory inducers, to stimulate cells in the vascular wall toinitiate the inflammatory process of atherosclerosis. Thissimulation may assist in evaluating drugs with potentialanti-atherosclerotic and anti-inflammatory actions, with the mostimportant stimulating factor being tumour necrosis factor (TNF)-α(–). In our previous study, wedemonstrated that TNF-α exhibits a number of effects as astimulator, however, TNF-α was not an ideal stimulator in thisEC-SMC-MC model.

Effect of Nonsteroid Anti-Inflammatory and Antipyretic Drugs on Prostaglandin Biosynthesis by Human Skin

Non-steroid anti-inflammatory drugs, prostaglandins, …

The preponderance of scientific evidence shows that NSAIDs damage articular cartilage. Various scientific papers and consensus groups have stated that there is no convincing data to show that the widely used NSAIDs and recommended selective COX-2 inhibitors have favorable effects on cartilage.129-131 Even the main consensus paper from the International Cartilage Repair Society and Osteoarthritis Research Society International stated that NSAID use has to be limited to the short term. Specifically the recommendation was as follows: In patients with symptomatic hip or knee osteoarthritis, non-steroidal anti-inflammatory drugs (NSAIDs) should be used at the lowest effective dose but their long-term use should be avoided if possible.132 They also noted that NSAIDs should not be first-line therapy for joint OA. Other groups have raised similar sentiments. The committees of the International League Against Rheumatism and the World Health Organization came up with guidelines for the testing of new drugs in osteoarthritis. The consensus from these meetings resulted in recommendations by The European Group for the Respect of Ethics and Excellence in Science (GREES) for governmental registration and approval of new drugs used in the treatment of OA and have added the requirement that the drug not have a deleterious effect on the diseased and non-diseased contra lateral joint; i.e., no deleterious effect on osteoarthritic or normal cartilage.133 If this latter recommendation were followed, the vast majority, if not all NSAIDs, would be immediately taken off the market and no new ones would get approved.