Anti-inflammatory effects NSAIDs

The anti-inflammatory effects of the NSAIDs are carried out by inhibition of COX-2. The gastrointestinal adverse reactions are caused by inhibition of COX-1. The newer NSAIDs (celecoxib and rofecoxib) appear to work by specifically inhibiting the COX-2 enzyme, without inhibiting the COX-1 enzyme. Celecoxib and rofecoxib relieve pain and inflammation with less potential for gastrointestinal adverse... 

NSAIDs are classified as non-selective (they inhibit COX-1 and COX-2) or selective (they inhibit only COX-2) based on degree of cyclooxygenase inhibition. COX-2 inhibition is responsible for anti-inflammatory effects, while COX-1 inhibition contributes to increased GI and renal toxicity associated with non-selective agents. Since the antiplatelet effect of non-selective NSAIDs is reversible, concurrent use may reduce the... 

However, it is important to note that the addition of nephrotoxic agents, such as amphotericin B, aminoglysides (e.g., gentamicin, tobramidn, or amikacin), and non-steroidal anti-inflammatory drugs (NSAIDs e.g., naproxen, ibuprofen, or ketorolac) may potentiate the nephrotoxic effects of the calcineurin inhibitors. 

In contrast, the COX-2 enzyme is not produced normally in most tissues, but its production is increased rapidly in the presence of inflammation and local tissue injury. This leads to the synthesis of prostaglandins involved in pain and inflammation. Consequently, blocking the COX-2 enzyme results in analgesic and anti-inflammatory effects. The beneficial effects of NSAIDs in reducing pain, decreasing joint stiffness, and improving function in patients with OA are thought to be due to inhibition of the COX-2 isoenzyme. 

In patients treated with acetaminophen or NSAIDs, assess pain control after 2 to 3 weeks. It may take longer for the full anti-inflammatory effect of NSAIDs to occur. 

NSAIDs are used commonly for musculoskeletal pain because of their availability without a prescription and anti-inflammatory effects.30,31 NSAIDs are a preferred choice over acetaminophen in musculoskeletal disorders where inflammation is evident.27 However, there is some controversy because the inflammatory response may be necessary for healing.13 Nevertheless, most experts recommend the use of NSAIDs early after acute injury to control inflammation and the range -of-motion limitations that may accompany swelling.27... 

Topical NSAIDs are available commercially in Canada and Europe. In the United States, these agents may be compounded in specialty pharmacies.35 These agents exert a local anti-inflammatory and analgesic effect.36-38 In soft-tissue injury such as strains and sprains, topical NSAIDs are superior in efficacy to placebo and similar to oral NSAIDs.36,37 Tissue concentrations of topical NSAIDs are high enough to produce anti-inflammatory effects, but systemic concentrations after application remain low.36-38... 

In addition to their beneficial effects, some medications may actually cause cellular injury and disease. An example of this phenomenon involves nonsteroidal anti-inflammatory drugs (NSAIDS). These drugs include aspirin (a derivative of salicylic acid), ibuprofen (arylpropionic acid, Advil ), and acetaminophen (para-aminophenol derivative, Tylenol ). Because of their beneficial pharmacological effects, consumption of these agents has increased significantly in recent years. NSAIDS have the ability to treat fever, pain, acute inflammation, and chronic inflammatory diseases such as arthritis. They are also used prophylactically to prevent heart disease, stroke, and colon cancer. 

Nonsteroidal anti-inflammatory drugs (NSAIDs) are widely prescribed medicines. Although these compounds represent a very effective class of drugs, their use is associ-... 

Non-steroidal anti-inflammatory drugs (NSAIDs), such as aspirin, were utilized primarily to protect from inflammation. Other biological effects were also found gradually, for example, induction of apoptosis [94, 95], stimulation of immune activity... 

COX-2 Inhibitor Celecoxib (Celebrex, Pfizer) inhibits the enzyme COX-2, which is involved in pain and inflammation, but it has no effect on the COX-1 enzyme, which helps to maintain stomach lining. It is prescribed for the relief of pain and symptoms of osteoarthritis and rheumatoid arthritis. Previously, nonsteroidal anti-inflammatory drugs (NSAIDs) were used. NSAIDs inhibit both COX-1 and COX-2 enzymes and cause stomach bleeding (see Case Study 2). 

Indometacin is an indole acetic acid derivative, while naproxen is a propionic acid derivative. Both are non-steroidal anti-inflammatory drugs (NSAIDs). Indometacin is associated with a higher incidence of side-effects, particularly gastrointestinal as well as headache and dizziness. 

Acetylsalicylic acid and related non-steroidal anti-inflammatory drugs (NSAIDs) selectively inhibit the cyclooxygenase activity of prostaglandin synthase [2] and consequently the synthesis of most eicosanoids. This explains their analgesic, antipyretic, and antirheumatic effects. Frequent side effects of NSAIDs also result from inhibition of eicosanoid synthesis. For example, they impair hemostasis because the synthesis of thromboxanes by thrombocytes is inhibited. In the stomach, NSAIDs increase HCl secretion and at the same time inhibit the formation of protective mucus. Long-term NSAID use can therefore damage the gastric mucosa. 

The anti-inflammatory effect of NSAIDs is achieved mainly through the inhibition of cyclooxygenases (COXs), key enzymes in prostaglandin (PG) biosynthesis from arachidonic acid. ... 

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