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Titolo:
MECHANISM OF ACTION OF ANTIINFLAMMATORY DRUGS
Autore:
VANE JR; BOTTING RM;
Indirizzi:
UNIV LONDON QUEEN MARY & WESTFIELD COLL,ST BARTHOLOMEWS & ROYAL LONDON SCH MED & DENT LONDON EC1M 6BQ ENGLAND
Titolo Testata:
International journal on tissue reactions
fascicolo: 1, volume: 20, anno: 1998,
pagine: 3 - 15
SICI:
0250-0868(1998)20:1<3:MOAOAD>2.0.ZU;2-K
Fonte:
ISI
Lingua:
ENG
Soggetto:
PROSTAGLANDIN G/H SYNTHASE-1; CYCLOOXYGENASE-2 MESSENGER-RNA; HUMAN CHORIONIC-GONADOTROPIN; HUMAN FETAL MEMBRANES; INDUCIBLE CYCLOOXYGENASE; SELECTIVE-INHIBITION; DIFFERENTIAL INHIBITION; ENDOPEROXIDE SYNTHASE; H SYNTHASE-2; GASTRIC-ULCERATION;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Citazioni:
94
Recensione:
Indirizzi per estratti:
Citazione:
J.R. Vane e R.M. Botting, "MECHANISM OF ACTION OF ANTIINFLAMMATORY DRUGS", International journal on tissue reactions, 20(1), 1998, pp. 3-15

Abstract

In 1971, Vane showed that nonsteroid antiinflammatory drugs (NSAIDs) inhibited the biosynthesis of prostaglandins and proposed this as their mechanism of action. Much work around the world has followed. The aspirin-like drugs inhibit the binding of the prostaglandin substrate, arachidonic acid, to the active site of the enzyme. After characterization of the COX-I enzyme in 1976, a second COX gene was discovered in 1991 encoding for the inducible COX-2. The constitutive isoform of COX,COX-1, has clear physiological functions. The inducible isoform, COX-2, is induced by pro-inflammatory stimuli in migratory cells and inflamed tissues. The range of activities of NSAIDs against COX-1 compared to COX-2 explains the variations in the side effects of NSAIDs at their antiinflammatory doses. Drugs which have the highest potency on COX-2 and less effect on COX-I will have potent antiinflammatory activity with fewer side effects. All the results published so far support ?he hypothesis that the unwanted side effects of NSAIDs, such as damage tothe gastric mucosa and kidneys, are due to their ability to inhibit COX-1, while their antiinflammatory (therapeutic effects) are due to inhibition of COX-2. Other roles for COX-2 inhibitors will surely be found in the next few years, for prostaglandin formation is under strong control in organs such as the kidney lungs and uterus. COX-2 is also potently expressed in human colon cancer cells, and NSAIDs delay the progress of colon tumors possibly by causing apoptosis of the tumor cells. The risk of developing Alzheimer's disease, which may involve an inflammatory component, is lessened by chronic ingestion of NSAIDs. The new highly selective inhibitors of COX-2 will not only provide a meansof delaying premature labor but will also lead to advances in cancer therapy and protection against Alzheimer's disease.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 13/08/20 alle ore 14:38:41