Selective Cyclooxygenase Inhibitors: Current Status

Abstract

For ages aspirin has established its value as an analgesic, anti-inflammatory drug, but in 1938, it was found to be a causative factor of gastric inflammation (ulcer). Later discovered non-steroidal anti-inflammatory drugs (NSAIDs) were found effective as aspirin but failed to overcome the goal of safer aspirin. As the method of prostaglandin inhibition through COX is a common mechanism to both the wanted and unwanted effects of aspirin and non-aspirin NSAIDs, the COX enzyme becomes a target for drug designers for the development of the "safe aspirin". In the late 1990s, a new class of drug molecules collectively known as selective inhibitors of cyclooxygenase-2(Coxibs) was developed for the treatment of pain and inflammation. Coxibs developed were as efficacious as the common NSAIDs, but they are devoid of major side effect, the gastrointestinal bleeding. This review presents an overview on all the discovered COX-2 inhibitors, their physiological role, side effects and reasons of their withdrawal.

NAC Attenuates LPS-Induced Toxicity in Aspirin-Sensitized Mouse Macrophages via Suppression of Oxidative Stress and Mitochondrial Dysfunction

“…Although aspirin is considered to be a specific inhibitor of PGs synthesis, its effect on COX is still controversial in different cell lines and its broad pharmacological effects may be associated through the regulation of redox metabolism, cell signaling and mitochondrial functions [14]–[15]. We, therefore, have studied the effects of LPS stimulation on murine macrophage J774.2 in conjunction with ASA.…”

Diffuse alveolar damage and acute kidney injury induced by abusive use of non-steroidal anti-inflammatory drugs: a new and atypical renopulmonary syndrome?

“…NSAID are known to inhibit prostaglandins and in addition, platelets aggregation, inflammation, vascular tone and permeability. 6,7 At normal or high dosages of NSAID, pulmonary capillaries are not affected, but our patient administered to himself an exceeding excessive dosage of ibuprofen whose clinical effects were unknown until that date.…”

Effect of ozone oxidative preconditioning on inflammation and oxidative stress injury in rat model of renal transplantation

“…Another well-know factor is COX-2, which is an inducible enzyme. Research showed that COX-2 expressed at sites of infection, inflammation and tumor which generated prostanoids that drive disease pathogenesis 29,30 . It has been showed that COX-2 can be rapidly and robustly expressed in response to diverse range of proinflammation cytokines and mediators 31 .…”