Serveur d'exploration sur le saule

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Development of GI-safe NSAID; progression from the bark of willow tree to modern pharmacology.

Identifieur interne : 001148 ( Main/Exploration ); précédent : 001147; suivant : 001149

Development of GI-safe NSAID; progression from the bark of willow tree to modern pharmacology.

Auteurs : Napapan Kangwan [Corée du Sud] ; Jong Min Park [Corée du Sud] ; Ki Baik Hahm [Corée du Sud]

Source :

RBID : pubmed:24956584

Descripteurs français

English descriptors

Abstract

Non-steroidal anti-inflammatory drugs (NSAIDs) have been used for analgesic, anti-inflammatory and antithrombotic actions and recently for cancer prevention, but they carries a risk of major gastroduodenal damages from symptomatic ulcers to serious complications leading to fatal outcomes. Therefore, the novel strategies to rescue long-term NSAID requiring patients from NSAID-associated gastroduodenal damages are essential. Besides of current drugs based on classic damaging mechanisms attributable to the decline of gastric mucosal prostaglandin synthesis, reductions of mucosal blood flow, attenuated bicarbonate secretion and mucus synthesis related with prostaglandin levels, effective therapeutics targeted for update mechanisms of NSAID-induced gastroduodenal damages are introduced in this paper based on recent advances in basic science and biotechnology exploring deeper molecular mechanisms of NSAID-induced gastroduodenal damage beyond COX inhibition.

DOI: 10.1016/j.coph.2014.06.003
PubMed: 24956584


Affiliations:


Links toward previous steps (curation, corpus...)


Le document en format XML

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<term>Anti-Inflammatory Agents, Non-Steroidal (therapeutic use)</term>
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<term>Maladies intestinales (induit chimiquement)</term>
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<term>Maladies intestinales (traitement médicamenteux)</term>
<term>Muqueuse gastrique (effets des médicaments et des substances chimiques)</term>
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<div type="abstract" xml:lang="en">Non-steroidal anti-inflammatory drugs (NSAIDs) have been used for analgesic, anti-inflammatory and antithrombotic actions and recently for cancer prevention, but they carries a risk of major gastroduodenal damages from symptomatic ulcers to serious complications leading to fatal outcomes. Therefore, the novel strategies to rescue long-term NSAID requiring patients from NSAID-associated gastroduodenal damages are essential. Besides of current drugs based on classic damaging mechanisms attributable to the decline of gastric mucosal prostaglandin synthesis, reductions of mucosal blood flow, attenuated bicarbonate secretion and mucus synthesis related with prostaglandin levels, effective therapeutics targeted for update mechanisms of NSAID-induced gastroduodenal damages are introduced in this paper based on recent advances in basic science and biotechnology exploring deeper molecular mechanisms of NSAID-induced gastroduodenal damage beyond COX inhibition. </div>
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