Non-steroidal anti-inflammatory drugs (NSAID) have long
been, and still, an essential group of drugs having anti-inflammatory,
antipyretic, and analgesic effects. The significant gastro-intestinal toxicity
associated with their use in treatment of
chronic arthritis remains of great
concern in clinical applications. The central pathogenic mechanism in
NSAID-induced gastro-duodenal toxicity lies in their ability to inhibit the
synthesis of prostaglandins by gastric mucosa through inhibition of cyclooxygenase
enzyme (Cox). There are two isoforms of Cox enzyme: Cox-1 and
Cox-2. The gastro-protective effects of prostaglandins are mediated by Cox-
1, while the inflammatory effects are mediated by Cox-2. NSAID lead to
inhibition of synthesis of prostaglandins, resulting in toxic effects on gastric
mucosa and beneficial anti-inflammatory effects.
