Development of GI-safe NSAID; progression from the bark of willow tree to modern pharmacology.
Identifieur interne : 001148 ( Main/Exploration ); précédent : 001147; suivant : 001149Development 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 :
- Current opinion in pharmacology [ 1471-4973 ] ; 2014.
Descripteurs français
- KwdFr :
- Agents protecteurs (pharmacologie), Agents protecteurs (usage thérapeutique), Animaux (MeSH), Anti-inflammatoires non stéroïdiens (effets indésirables), Anti-inflammatoires non stéroïdiens (pharmacologie), Anti-inflammatoires non stéroïdiens (usage thérapeutique), Humains (MeSH), Maladies intestinales (induit chimiquement), Maladies intestinales (prévention et contrôle), Maladies intestinales (traitement médicamenteux), Muqueuse gastrique (effets des médicaments et des substances chimiques), Salix (MeSH), Écorce (MeSH).
- MESH :
- effets des médicaments et des substances chimiques : Muqueuse gastrique.
- effets indésirables : Anti-inflammatoires non stéroïdiens.
- induit chimiquement : Maladies intestinales.
- pharmacologie : Agents protecteurs, Anti-inflammatoires non stéroïdiens.
- prévention et contrôle : Maladies intestinales.
- traitement médicamenteux : Maladies intestinales.
- usage thérapeutique : Agents protecteurs, Anti-inflammatoires non stéroïdiens.
- Animaux, Humains, Salix, Écorce.
English descriptors
- KwdEn :
- Animals (MeSH), Anti-Inflammatory Agents, Non-Steroidal (adverse effects), Anti-Inflammatory Agents, Non-Steroidal (pharmacology), Anti-Inflammatory Agents, Non-Steroidal (therapeutic use), Gastric Mucosa (drug effects), Humans (MeSH), Intestinal Diseases (chemically induced), Intestinal Diseases (drug therapy), Intestinal Diseases (prevention & control), Plant Bark (MeSH), Protective Agents (pharmacology), Protective Agents (therapeutic use), Salix (MeSH).
- MESH :
- chemical , adverse effects : Anti-Inflammatory Agents, Non-Steroidal.
- chemical , pharmacology : Anti-Inflammatory Agents, Non-Steroidal, Protective Agents.
- chemical , therapeutic use : Anti-Inflammatory Agents, Non-Steroidal, Protective Agents.
- chemically induced : Intestinal Diseases.
- drug effects : Gastric Mucosa.
- drug therapy : Intestinal Diseases.
- prevention & control : Intestinal Diseases.
- Animals, Humans, Plant Bark, Salix.
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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<front><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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