PAIN RELIF NON-STEROIDAL

Pain Relief Using Non-Steroidal Anti-Inflammatory Drugs

Pain Relief Using Non-Steroidal Anti-Inflammatory Drugs

Introduction

Previous term Non-steroidal anti-inflammatory drugs (NSAIDs) next term are frequently used to treat inflammation and pain in a wide variety of disorders. The best-known mechanism underlying the action of previous term NSAIDs next term is the inhibition of prostaglandin synthesis secondary to their action on cyclooxygenases (COXs). It is well known that clinical treatment with previous term NSAIDs next term carries a significant risk of both gastric and duodenal ulcers (Sakamoto, 2003). Moreover, previous term NSAIDs next term such as indomethacin and diclofenac produce gastrointestinal mucosal injuries in experimental animals (Allison, 1992). Recent reports suggest that the detrimental effects of previous term NSAIDs next term are attributable to cellular proliferation, cell cycle progression, and apoptosis (Slomiany et al., 1997 B.L. Slomiany, J. Piotrowski and A. Slomiany, Induction of tumor necrosis factor-alpha and apoptosis in gastric mucosal injury by indomethacin. Effect of omeprazole and ebrotidine, Scandinavian Journal of Gastroenterology 32 (1997), pp. 638-642. (59)Slomiany et al., 1997, Slomiany et al., 1999 and Piotrowski et al., 1999). Indeed, previous term NSAIDs next term induce direct apoptosis of cultured rat gastric mucosal cells (Kusuhara et al., 1998). In many recent reports, previous term NSAIDs next term exert apoptotic effects against a variety of cell lines other than gastric mucosal cells, such as colon cancer cells. On the other hand, few reports show previous termNSAIDs having antinext term-apoptotic effects. previous term NSAIDs next term such as nimesulide and ibuprofen show protective effects in osteoarthritis through the inhibition of apoptosis in chondrocytes (Mukherjee et al., 2001). Aspirin prevents apoptosis induced by H2O2 in HeLa cells (Kutuk and Basaga, 2003). Furthermore, a low dose of NS-398, a selective cyclooxygenase-2 inhibitor, induces a marked decrease in apoptosis in human 1547 osteosarcoma cells (Moalic, 2001). Thus, the involvement of previous term NSAIDs next term on cell apoptosis is so complicated that the underlying mechanisms have not been well defined.

Discussion

Previous term NSAIDs next term are frequently used to treat rheumatoid arthritis because of their analgesic and previous termanti inflammatory next term activities. A major mechanism underlying the action of previous term NSAIDs next term is generally thought to be the inhibition of COX (Vane, 1971). COX is a key enzyme in catalyzing the conversion of arachidonic acid, which is released from the cell membrane, into prostaglandin G2 and prostaglandin H2. There are two isoforms of COX: COX-1 and COX-2 (Kujubu et al., 1991 and Xie et al., 1991). Recent evidence suggests that previous term NSAIDs next term exert apoptotic effects in a variety of cell lines, including colon cancer cells. On the other hand, a few papers have reported on the previous termanti next term-apoptotic effects of previous term NSAIDs next term). The involvement of previous term NSAIDs next term on cell apoptosis is so complicated that the mechanism underlying previous term NSAID next term apoptosis has not been well defined.

Protein misfolding and the accumulation of unfolded proteins can result from the inhibition of protein glycosylation, ...