Development of GI-safe NSAID; progression from the bark of willow tree to modern pharmacology.
Identifieur interne : 001086 ( Main/Corpus ); précédent : 001085; suivant : 001087Development of GI-safe NSAID; progression from the bark of willow tree to modern pharmacology.
Auteurs : Napapan Kangwan ; Jong Min Park ; Ki Baik HahmSource :
- Current opinion in pharmacology [ 1471-4973 ] ; 2014.
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
Links to Exploration step
pubmed:24956584Le document en format XML
<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Development of GI-safe NSAID; progression from the bark of willow tree to modern pharmacology.</title><author><name sortKey="Kangwan, Napapan" sort="Kangwan, Napapan" uniqKey="Kangwan N" first="Napapan" last="Kangwan">Napapan Kangwan</name><affiliation><nlm:affiliation>CHA Cancer Prevention Research Center, CHA Cancer Institute, CHA University, Seoul 135-081, Republic of Korea.</nlm:affiliation></affiliation></author><author><name sortKey="Park, Jong Min" sort="Park, Jong Min" uniqKey="Park J" first="Jong Min" last="Park">Jong Min Park</name><affiliation><nlm:affiliation>CHA Cancer Prevention Research Center, CHA Cancer Institute, CHA University, Seoul 135-081, Republic of Korea.</nlm:affiliation></affiliation></author><author><name sortKey="Hahm, Ki Baik" sort="Hahm, Ki Baik" uniqKey="Hahm K" first="Ki Baik" last="Hahm">Ki Baik Hahm</name><affiliation><nlm:affiliation>CHA Cancer Prevention Research Center, CHA Cancer Institute, CHA University, Seoul 135-081, Republic of Korea; CHA University Bundang Medical Center, Digestive Disease Center, Seongnam 463-712, Republic of Korea. Electronic address: hahmkb@cha.ac.kr.</nlm:affiliation></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2014">2014</date><idno type="RBID">pubmed:24956584</idno><idno type="pmid">24956584</idno><idno type="doi">10.1016/j.coph.2014.06.003</idno><idno type="wicri:Area/Main/Corpus">001086</idno><idno type="wicri:explorRef" wicri:stream="Main" wicri:step="Corpus" wicri:corpus="PubMed">001086</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Development of GI-safe NSAID; progression from the bark of willow tree to modern pharmacology.</title><author><name sortKey="Kangwan, Napapan" sort="Kangwan, Napapan" uniqKey="Kangwan N" first="Napapan" last="Kangwan">Napapan Kangwan</name><affiliation><nlm:affiliation>CHA Cancer Prevention Research Center, CHA Cancer Institute, CHA University, Seoul 135-081, Republic of Korea.</nlm:affiliation></affiliation></author><author><name sortKey="Park, Jong Min" sort="Park, Jong Min" uniqKey="Park J" first="Jong Min" last="Park">Jong Min Park</name><affiliation><nlm:affiliation>CHA Cancer Prevention Research Center, CHA Cancer Institute, CHA University, Seoul 135-081, Republic of Korea.</nlm:affiliation></affiliation></author><author><name sortKey="Hahm, Ki Baik" sort="Hahm, Ki Baik" uniqKey="Hahm K" first="Ki Baik" last="Hahm">Ki Baik Hahm</name><affiliation><nlm:affiliation>CHA Cancer Prevention Research Center, CHA Cancer Institute, CHA University, Seoul 135-081, Republic of Korea; CHA University Bundang Medical Center, Digestive Disease Center, Seongnam 463-712, Republic of Korea. Electronic address: hahmkb@cha.ac.kr.</nlm:affiliation></affiliation></author></analytic><series><title level="j">Current opinion in pharmacology</title><idno type="eISSN">1471-4973</idno><imprint><date when="2014" type="published">2014</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals (MeSH)</term><term>Anti-Inflammatory Agents, Non-Steroidal (adverse effects)</term><term>Anti-Inflammatory Agents, Non-Steroidal (pharmacology)</term><term>Anti-Inflammatory Agents, Non-Steroidal (therapeutic use)</term><term>Gastric Mucosa (drug effects)</term><term>Humans (MeSH)</term><term>Intestinal Diseases (chemically induced)</term><term>Intestinal Diseases (drug therapy)</term><term>Intestinal Diseases (prevention & control)</term><term>Plant Bark (MeSH)</term><term>Protective Agents (pharmacology)</term><term>Protective Agents (therapeutic use)</term><term>Salix (MeSH)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="adverse effects" xml:lang="en"><term>Anti-Inflammatory Agents, Non-Steroidal</term></keywords><keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Anti-Inflammatory Agents, Non-Steroidal</term><term>Protective Agents</term></keywords><keywords scheme="MESH" type="chemical" qualifier="therapeutic use" xml:lang="en"><term>Anti-Inflammatory Agents, Non-Steroidal</term><term>Protective Agents</term></keywords><keywords scheme="MESH" qualifier="chemically induced" xml:lang="en"><term>Intestinal Diseases</term></keywords><keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Gastric Mucosa</term></keywords><keywords scheme="MESH" qualifier="drug therapy" xml:lang="en"><term>Intestinal Diseases</term></keywords><keywords scheme="MESH" qualifier="prevention & control" xml:lang="en"><term>Intestinal Diseases</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Humans</term><term>Plant Bark</term><term>Salix</term></keywords></textClass></profileDesc></teiHeader><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></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">24956584</PMID><DateCompleted><Year>2015</Year><Month>08</Month><Day>04</Day></DateCompleted><DateRevised><Year>2014</Year><Month>12</Month><Day>02</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1471-4973</ISSN><JournalIssue CitedMedium="Internet"><Volume>19</Volume><PubDate><Year>2014</Year><Month>Dec</Month></PubDate></JournalIssue><Title>Current opinion in pharmacology</Title><ISOAbbreviation>Curr Opin Pharmacol</ISOAbbreviation></Journal><ArticleTitle>Development of GI-safe NSAID; progression from the bark of willow tree to modern pharmacology.</ArticleTitle><Pagination><MedlinePgn>17-23</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1016/j.coph.2014.06.003</ELocationID><ELocationID EIdType="pii" ValidYN="Y">S1471-4892(14)00054-X</ELocationID><Abstract><AbstractText>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. </AbstractText><CopyrightInformation>Copyright © 2014. Published by Elsevier Ltd.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Kangwan</LastName><ForeName>Napapan</ForeName><Initials>N</Initials><AffiliationInfo><Affiliation>CHA Cancer Prevention Research Center, CHA Cancer Institute, CHA University, Seoul 135-081, Republic of Korea.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Park</LastName><ForeName>Jong Min</ForeName><Initials>JM</Initials><AffiliationInfo><Affiliation>CHA Cancer Prevention Research Center, CHA Cancer Institute, CHA University, Seoul 135-081, Republic of Korea.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Hahm</LastName><ForeName>Ki Baik</ForeName><Initials>KB</Initials><AffiliationInfo><Affiliation>CHA Cancer Prevention Research Center, CHA Cancer Institute, CHA University, Seoul 135-081, Republic of Korea; CHA University Bundang Medical Center, Digestive Disease Center, Seongnam 463-712, Republic of Korea. Electronic address: hahmkb@cha.ac.kr.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType><PublicationType UI="D016454">Review</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2014</Year><Month>06</Month><Day>21</Day></ArticleDate></Article><MedlineJournalInfo><Country>England</Country><MedlineTA>Curr Opin Pharmacol</MedlineTA><NlmUniqueID>100966133</NlmUniqueID><ISSNLinking>1471-4892</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D000894">Anti-Inflammatory Agents, Non-Steroidal</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D020011">Protective Agents</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000894" MajorTopicYN="Y">Anti-Inflammatory Agents, Non-Steroidal</DescriptorName><QualifierName UI="Q000009" MajorTopicYN="N">adverse effects</QualifierName><QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName><QualifierName UI="Q000627" MajorTopicYN="N">therapeutic use</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D005753" MajorTopicYN="N">Gastric Mucosa</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D007410" MajorTopicYN="N">Intestinal Diseases</DescriptorName><QualifierName UI="Q000139" MajorTopicYN="N">chemically induced</QualifierName><QualifierName UI="Q000188" MajorTopicYN="N">drug therapy</QualifierName><QualifierName UI="Q000517" MajorTopicYN="N">prevention & control</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D024301" MajorTopicYN="N">Plant Bark</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D020011" MajorTopicYN="N">Protective Agents</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName><QualifierName UI="Q000627" MajorTopicYN="N">therapeutic use</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D032108" MajorTopicYN="N">Salix</DescriptorName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2014</Year><Month>05</Month><Day>28</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2014</Year><Month>06</Month><Day>01</Day></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2014</Year><Month>6</Month><Day>24</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2014</Year><Month>6</Month><Day>24</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2015</Year><Month>8</Month><Day>5</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">24956584</ArticleId><ArticleId IdType="pii">S1471-4892(14)00054-X</ArticleId><ArticleId IdType="doi">10.1016/j.coph.2014.06.003</ArticleId></ArticleIdList></PubmedData></pubmed></record>Pour manipuler ce document sous Unix (Dilib)
EXPLOR_STEP=$WICRI_ROOT/Bois/explor/WillowV1/Data/Main/Corpus
HfdSelect -h $EXPLOR_STEP/biblio.hfd -nk 001086 | SxmlIndent | more
Ou
HfdSelect -h $EXPLOR_AREA/Data/Main/Corpus/biblio.hfd -nk 001086 | SxmlIndent | more
Pour mettre un lien sur cette page dans le réseau Wicri
{{Explor lien
|wiki= Bois
|area= WillowV1
|flux= Main
|étape= Corpus
|type= RBID
|clé= pubmed:24956584
|texte= Development of GI-safe NSAID; progression from the bark of willow tree to modern pharmacology.
}}
Pour générer des pages wiki
HfdIndexSelect -h $EXPLOR_AREA/Data/Main/Corpus/RBID.i -Sk "pubmed:24956584" \
| HfdSelect -Kh $EXPLOR_AREA/Data/Main/Corpus/biblio.hfd \
| NlmPubMed2Wicri -a WillowV1
| This area was generated with Dilib version V0.6.37. |  |