The biochemical protective mechanisms against non-steroidal anti-inflammatory drug induced G-I mucosal damage.
Conventional anti-ulcer agents give some protection against NSAID-induced GI injury, but they are by no means totally effective nor without some disadvantage for their side effects cost and for lack of efficacy. More selective protective effects may be achieved by use of agents which counteract the biochemical and cytological changes induced by the NSAIDs. The relative success of these approaches has yet to be fully evaluated but at least some of these procedures may prove cheaper and devoid of side effects encountered with traditional anti-ulcer therapies.
Rainsford
K D
KD
Anti-Inflammatory Research Unit, Strangeways Research Laboratory, England.
D000255:Adenosine Triphosphate / Q000378:metabolism; D000818:Animals; D000863:Antacids / Q000627:therapeutic use; D000894:Anti-Inflammatory Agents, Non-Steroidal / Q000009:adverse effects* / Q000037:antagonists & inhibitors; D002413:Cations, Divalent; D005609:Free Radicals; D005744:Gastric Acid / Q000378:metabolism; D005753:Gastric Mucosa / Q000187:drug effects*; D006801:Humans; D007413:Intestinal Mucosa / Q000187:drug effects*; D008084:Lipoxygenase / Q000378:metabolism; D010437:Peptic Ulcer / Q000139:chemically induced / Q000517:prevention & control*; D011453:Prostaglandins / Q000627:therapeutic use
D000863:Antacids; D000894:Anti-Inflammatory Agents, Non-Steroidal; D002413:Cations, Divalent; D005609:Free Radicals; D011453:Prostaglandins; D000255:Adenosine Triphosphate; D008084:Lipoxygenase