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Effects of ibuprofen enantiomers and its coenzyme A thioesters on human prostaglandin endoperoxide synthases
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| Zeitschriftentitel: | British Journal of Pharmacology |
|---|---|
| Personen und Körperschaften: | , , , , |
| In: | British Journal of Pharmacology, 122, 1997, 3, S. 487-492 |
| Format: | E-Article |
| Sprache: | Englisch |
| veröffentlicht: |
Wiley
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| Schlagwörter: |
| author_facet |
Neupert, Werner Brugger, Roland Euchenhofer, Christian Brune, Kay Geisslinger, Gerd Neupert, Werner Brugger, Roland Euchenhofer, Christian Brune, Kay Geisslinger, Gerd |
|---|---|
| author |
Neupert, Werner Brugger, Roland Euchenhofer, Christian Brune, Kay Geisslinger, Gerd |
| spellingShingle |
Neupert, Werner Brugger, Roland Euchenhofer, Christian Brune, Kay Geisslinger, Gerd British Journal of Pharmacology Effects of ibuprofen enantiomers and its coenzyme A thioesters on human prostaglandin endoperoxide synthases Pharmacology |
| author_sort |
neupert, werner |
| spelling |
Neupert, Werner Brugger, Roland Euchenhofer, Christian Brune, Kay Geisslinger, Gerd 0007-1188 1476-5381 Wiley Pharmacology http://dx.doi.org/10.1038/sj.bjp.0701415 <jats:p> <jats:list list-type="explicit-label"> <jats:list-item><jats:p>Ibuprofen enantiomers and their respective coenzyme A thioesters were tested in human platelets and blood monocytes to determine their selectivity and potency as inhibitors of cyclo‐oxygenase activity of prostaglandin endoperoxide synthase‐1 (PGHS‐1) and PGHS‐2.</jats:p></jats:list-item> <jats:list-item><jats:p>Human blood from volunteers was drawn and allowed to clot at 37°C for 1 h in the presence of increasing concentrations of the test compounds (<jats:bold>R</jats:bold>‐ibuprofen, <jats:bold>S</jats:bold>‐ibuprofen, <jats:bold>R</jats:bold>‐ibuprofenoyl‐CoA, <jats:bold>S</jats:bold>‐ibuprofenoyl‐CoA, NS‐398). Immunoreactive (ir) thromboxane B<jats:sub>2</jats:sub> (TXB<jats:sub>2</jats:sub>) concentrations in serum were determined by a specific EIA assay as an index of the cyclo‐oxygenase activity of platelet PGHS‐1.</jats:p></jats:list-item> <jats:list-item><jats:p>Heparin‐treated blood from the same donors was incubated at 37°C for 24 h with the same concentrations of the test compounds in the presence of lipopolysaccharide (LPS, 10 μg ml<jats:sup>−1</jats:sup>). The contribution of PGHS‐1 was suppressed by pretreatment of the volunteers with aspirin (500 mg; 48 h before venepuncture). As a measure of LPS induced PGHS‐2 activity immunoreactive prostaglandin E<jats:sub>2</jats:sub> (irPGE<jats:sub>2</jats:sub>) plasma concentrations were determined by a specific EIA assay.</jats:p></jats:list-item> <jats:list-item><jats:p><jats:bold>S</jats:bold>‐ibuprofen inhibited the activity of PGHS‐1 (IC<jats:sub>50</jats:sub> 2.1 μ<jats:sc>M</jats:sc>) and PGHS‐2 (IC<jats:sub>50</jats:sub> 1.6 μ<jats:sc>M</jats:sc>) equally. <jats:bold>R</jats:bold>‐ibuprofen inhibited PGHS‐1 (IC<jats:sub>50</jats:sub> 34.9) less potently than <jats:bold>S</jats:bold>‐ibuprofen and showed no inhibition of PGHS‐2 up to 250 μ<jats:sc>M</jats:sc>. By contrast <jats:bold>R</jats:bold>‐ibuprofenoyl‐CoA thioester inhibited PGE<jats:sub>2</jats:sub> production from LPS‐stimulated monocytes almost two orders of magnitude more potently than the generation of TXB<jats:sub>2</jats:sub> (IC<jats:sub>50</jats:sub> 5.6 vs 219 μ<jats:sc>M</jats:sc>).</jats:p></jats:list-item> <jats:list-item><jats:p>Western blotting of PGHS‐2 after LPS induction of blood monocytes showed a concentration‐dependent inhibition of PGHS‐2 protein expression by ibuprofenoyl‐CoA thioesters.</jats:p></jats:list-item> <jats:list-item><jats:p>These data confirm that <jats:bold>S</jats:bold>‐ibuprofen represents the active entity in the racemate with respect to cyclo‐oxygenase activity. More importantly the data suggest a contribution of the <jats:bold>R</jats:bold>‐enantiomer to therapeutic effects not only by chiral inversion to <jats:bold>S</jats:bold>‐ibuprofen but also via inhibition of induction of PGHS‐2 mediated by <jats:bold>R</jats:bold>‐ibuprofenoyl‐CoA thioester.</jats:p></jats:list-item> <jats:list-item><jats:p>The data may explain why racemic ibuprofen is ranked as one of the safest non‐steroidal anti‐inflammatory drugs (NSAIDs) so far determined in epidemiological studies.</jats:p></jats:list-item> </jats:list> </jats:p><jats:p><jats:italic>British Journal of Pharmacology</jats:italic> (1997) <jats:bold>122</jats:bold>, 487–492; doi:<jats:ext-link xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" xlink:href="10.1038/sj.bjp.0701415">10.1038/sj.bjp.0701415</jats:ext-link></jats:p> Effects of ibuprofen enantiomers and its coenzyme A thioesters on human prostaglandin endoperoxide synthases British Journal of Pharmacology |
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neupert1997effectsofibuprofenenantiomersanditscoenzymeathioestersonhumanprostaglandinendoperoxidesynthases |
| publishDateSort |
1997 |
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Wiley |
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ai |
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ai |
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British Journal of Pharmacology |
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49 |
| title |
Effects of ibuprofen enantiomers and its coenzyme A thioesters on human prostaglandin endoperoxide synthases |
| title_unstemmed |
Effects of ibuprofen enantiomers and its coenzyme A thioesters on human prostaglandin endoperoxide synthases |
| title_full |
Effects of ibuprofen enantiomers and its coenzyme A thioesters on human prostaglandin endoperoxide synthases |
| title_fullStr |
Effects of ibuprofen enantiomers and its coenzyme A thioesters on human prostaglandin endoperoxide synthases |
| title_full_unstemmed |
Effects of ibuprofen enantiomers and its coenzyme A thioesters on human prostaglandin endoperoxide synthases |
| title_short |
Effects of ibuprofen enantiomers and its coenzyme A thioesters on human prostaglandin endoperoxide synthases |
| title_sort |
effects of ibuprofen enantiomers and its coenzyme a thioesters on human prostaglandin endoperoxide synthases |
| topic |
Pharmacology |
| url |
http://dx.doi.org/10.1038/sj.bjp.0701415 |
| publishDate |
1997 |
| physical |
487-492 |
| description |
<jats:p>
<jats:list list-type="explicit-label">
<jats:list-item><jats:p>Ibuprofen enantiomers and their respective coenzyme A thioesters were tested in human platelets and blood monocytes to determine their selectivity and potency as inhibitors of cyclo‐oxygenase activity of prostaglandin endoperoxide synthase‐1 (PGHS‐1) and PGHS‐2.</jats:p></jats:list-item>
<jats:list-item><jats:p>Human blood from volunteers was drawn and allowed to clot at 37°C for 1 h in the presence of increasing concentrations of the test compounds (<jats:bold>R</jats:bold>‐ibuprofen, <jats:bold>S</jats:bold>‐ibuprofen, <jats:bold>R</jats:bold>‐ibuprofenoyl‐CoA, <jats:bold>S</jats:bold>‐ibuprofenoyl‐CoA, NS‐398). Immunoreactive (ir) thromboxane B<jats:sub>2</jats:sub> (TXB<jats:sub>2</jats:sub>) concentrations in serum were determined by a specific EIA assay as an index of the cyclo‐oxygenase activity of platelet PGHS‐1.</jats:p></jats:list-item>
<jats:list-item><jats:p>Heparin‐treated blood from the same donors was incubated at 37°C for 24 h with the same concentrations of the test compounds in the presence of lipopolysaccharide (LPS, 10 μg ml<jats:sup>−1</jats:sup>). The contribution of PGHS‐1 was suppressed by pretreatment of the volunteers with aspirin (500 mg; 48 h before venepuncture). As a measure of LPS induced PGHS‐2 activity immunoreactive prostaglandin E<jats:sub>2</jats:sub> (irPGE<jats:sub>2</jats:sub>) plasma concentrations were determined by a specific EIA assay.</jats:p></jats:list-item>
<jats:list-item><jats:p><jats:bold>S</jats:bold>‐ibuprofen inhibited the activity of PGHS‐1 (IC<jats:sub>50</jats:sub> 2.1 μ<jats:sc>M</jats:sc>) and PGHS‐2 (IC<jats:sub>50</jats:sub> 1.6 μ<jats:sc>M</jats:sc>) equally. <jats:bold>R</jats:bold>‐ibuprofen inhibited PGHS‐1 (IC<jats:sub>50</jats:sub> 34.9) less potently than <jats:bold>S</jats:bold>‐ibuprofen and showed no inhibition of PGHS‐2 up to 250 μ<jats:sc>M</jats:sc>. By contrast <jats:bold>R</jats:bold>‐ibuprofenoyl‐CoA thioester inhibited PGE<jats:sub>2</jats:sub> production from LPS‐stimulated monocytes almost two orders of magnitude more potently than the generation of TXB<jats:sub>2</jats:sub> (IC<jats:sub>50</jats:sub> 5.6 vs 219 μ<jats:sc>M</jats:sc>).</jats:p></jats:list-item>
<jats:list-item><jats:p>Western blotting of PGHS‐2 after LPS induction of blood monocytes showed a concentration‐dependent inhibition of PGHS‐2 protein expression by ibuprofenoyl‐CoA thioesters.</jats:p></jats:list-item>
<jats:list-item><jats:p>These data confirm that <jats:bold>S</jats:bold>‐ibuprofen represents the active entity in the racemate with respect to cyclo‐oxygenase activity. More importantly the data suggest a contribution of the <jats:bold>R</jats:bold>‐enantiomer to therapeutic effects not only by chiral inversion to <jats:bold>S</jats:bold>‐ibuprofen but also via inhibition of induction of PGHS‐2 mediated by <jats:bold>R</jats:bold>‐ibuprofenoyl‐CoA thioester.</jats:p></jats:list-item>
<jats:list-item><jats:p>The data may explain why racemic ibuprofen is ranked as one of the safest non‐steroidal anti‐inflammatory drugs (NSAIDs) so far determined in epidemiological studies.</jats:p></jats:list-item>
</jats:list>
</jats:p><jats:p><jats:italic>British Journal of Pharmacology</jats:italic> (1997) <jats:bold>122</jats:bold>, 487–492; doi:<jats:ext-link xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" xlink:href="10.1038/sj.bjp.0701415">10.1038/sj.bjp.0701415</jats:ext-link></jats:p> |
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| author | Neupert, Werner, Brugger, Roland, Euchenhofer, Christian, Brune, Kay, Geisslinger, Gerd |
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| description | <jats:p> <jats:list list-type="explicit-label"> <jats:list-item><jats:p>Ibuprofen enantiomers and their respective coenzyme A thioesters were tested in human platelets and blood monocytes to determine their selectivity and potency as inhibitors of cyclo‐oxygenase activity of prostaglandin endoperoxide synthase‐1 (PGHS‐1) and PGHS‐2.</jats:p></jats:list-item> <jats:list-item><jats:p>Human blood from volunteers was drawn and allowed to clot at 37°C for 1 h in the presence of increasing concentrations of the test compounds (<jats:bold>R</jats:bold>‐ibuprofen, <jats:bold>S</jats:bold>‐ibuprofen, <jats:bold>R</jats:bold>‐ibuprofenoyl‐CoA, <jats:bold>S</jats:bold>‐ibuprofenoyl‐CoA, NS‐398). Immunoreactive (ir) thromboxane B<jats:sub>2</jats:sub> (TXB<jats:sub>2</jats:sub>) concentrations in serum were determined by a specific EIA assay as an index of the cyclo‐oxygenase activity of platelet PGHS‐1.</jats:p></jats:list-item> <jats:list-item><jats:p>Heparin‐treated blood from the same donors was incubated at 37°C for 24 h with the same concentrations of the test compounds in the presence of lipopolysaccharide (LPS, 10 μg ml<jats:sup>−1</jats:sup>). The contribution of PGHS‐1 was suppressed by pretreatment of the volunteers with aspirin (500 mg; 48 h before venepuncture). As a measure of LPS induced PGHS‐2 activity immunoreactive prostaglandin E<jats:sub>2</jats:sub> (irPGE<jats:sub>2</jats:sub>) plasma concentrations were determined by a specific EIA assay.</jats:p></jats:list-item> <jats:list-item><jats:p><jats:bold>S</jats:bold>‐ibuprofen inhibited the activity of PGHS‐1 (IC<jats:sub>50</jats:sub> 2.1 μ<jats:sc>M</jats:sc>) and PGHS‐2 (IC<jats:sub>50</jats:sub> 1.6 μ<jats:sc>M</jats:sc>) equally. <jats:bold>R</jats:bold>‐ibuprofen inhibited PGHS‐1 (IC<jats:sub>50</jats:sub> 34.9) less potently than <jats:bold>S</jats:bold>‐ibuprofen and showed no inhibition of PGHS‐2 up to 250 μ<jats:sc>M</jats:sc>. By contrast <jats:bold>R</jats:bold>‐ibuprofenoyl‐CoA thioester inhibited PGE<jats:sub>2</jats:sub> production from LPS‐stimulated monocytes almost two orders of magnitude more potently than the generation of TXB<jats:sub>2</jats:sub> (IC<jats:sub>50</jats:sub> 5.6 vs 219 μ<jats:sc>M</jats:sc>).</jats:p></jats:list-item> <jats:list-item><jats:p>Western blotting of PGHS‐2 after LPS induction of blood monocytes showed a concentration‐dependent inhibition of PGHS‐2 protein expression by ibuprofenoyl‐CoA thioesters.</jats:p></jats:list-item> <jats:list-item><jats:p>These data confirm that <jats:bold>S</jats:bold>‐ibuprofen represents the active entity in the racemate with respect to cyclo‐oxygenase activity. More importantly the data suggest a contribution of the <jats:bold>R</jats:bold>‐enantiomer to therapeutic effects not only by chiral inversion to <jats:bold>S</jats:bold>‐ibuprofen but also via inhibition of induction of PGHS‐2 mediated by <jats:bold>R</jats:bold>‐ibuprofenoyl‐CoA thioester.</jats:p></jats:list-item> <jats:list-item><jats:p>The data may explain why racemic ibuprofen is ranked as one of the safest non‐steroidal anti‐inflammatory drugs (NSAIDs) so far determined in epidemiological studies.</jats:p></jats:list-item> </jats:list> </jats:p><jats:p><jats:italic>British Journal of Pharmacology</jats:italic> (1997) <jats:bold>122</jats:bold>, 487–492; doi:<jats:ext-link xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" xlink:href="10.1038/sj.bjp.0701415">10.1038/sj.bjp.0701415</jats:ext-link></jats:p> |
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| imprint_str_mv | Wiley, 1997 |
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| match_str | neupert1997effectsofibuprofenenantiomersanditscoenzymeathioestersonhumanprostaglandinendoperoxidesynthases |
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| physical | 487-492 |
| publishDate | 1997 |
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| spelling | Neupert, Werner Brugger, Roland Euchenhofer, Christian Brune, Kay Geisslinger, Gerd 0007-1188 1476-5381 Wiley Pharmacology http://dx.doi.org/10.1038/sj.bjp.0701415 <jats:p> <jats:list list-type="explicit-label"> <jats:list-item><jats:p>Ibuprofen enantiomers and their respective coenzyme A thioesters were tested in human platelets and blood monocytes to determine their selectivity and potency as inhibitors of cyclo‐oxygenase activity of prostaglandin endoperoxide synthase‐1 (PGHS‐1) and PGHS‐2.</jats:p></jats:list-item> <jats:list-item><jats:p>Human blood from volunteers was drawn and allowed to clot at 37°C for 1 h in the presence of increasing concentrations of the test compounds (<jats:bold>R</jats:bold>‐ibuprofen, <jats:bold>S</jats:bold>‐ibuprofen, <jats:bold>R</jats:bold>‐ibuprofenoyl‐CoA, <jats:bold>S</jats:bold>‐ibuprofenoyl‐CoA, NS‐398). Immunoreactive (ir) thromboxane B<jats:sub>2</jats:sub> (TXB<jats:sub>2</jats:sub>) concentrations in serum were determined by a specific EIA assay as an index of the cyclo‐oxygenase activity of platelet PGHS‐1.</jats:p></jats:list-item> <jats:list-item><jats:p>Heparin‐treated blood from the same donors was incubated at 37°C for 24 h with the same concentrations of the test compounds in the presence of lipopolysaccharide (LPS, 10 μg ml<jats:sup>−1</jats:sup>). The contribution of PGHS‐1 was suppressed by pretreatment of the volunteers with aspirin (500 mg; 48 h before venepuncture). As a measure of LPS induced PGHS‐2 activity immunoreactive prostaglandin E<jats:sub>2</jats:sub> (irPGE<jats:sub>2</jats:sub>) plasma concentrations were determined by a specific EIA assay.</jats:p></jats:list-item> <jats:list-item><jats:p><jats:bold>S</jats:bold>‐ibuprofen inhibited the activity of PGHS‐1 (IC<jats:sub>50</jats:sub> 2.1 μ<jats:sc>M</jats:sc>) and PGHS‐2 (IC<jats:sub>50</jats:sub> 1.6 μ<jats:sc>M</jats:sc>) equally. <jats:bold>R</jats:bold>‐ibuprofen inhibited PGHS‐1 (IC<jats:sub>50</jats:sub> 34.9) less potently than <jats:bold>S</jats:bold>‐ibuprofen and showed no inhibition of PGHS‐2 up to 250 μ<jats:sc>M</jats:sc>. By contrast <jats:bold>R</jats:bold>‐ibuprofenoyl‐CoA thioester inhibited PGE<jats:sub>2</jats:sub> production from LPS‐stimulated monocytes almost two orders of magnitude more potently than the generation of TXB<jats:sub>2</jats:sub> (IC<jats:sub>50</jats:sub> 5.6 vs 219 μ<jats:sc>M</jats:sc>).</jats:p></jats:list-item> <jats:list-item><jats:p>Western blotting of PGHS‐2 after LPS induction of blood monocytes showed a concentration‐dependent inhibition of PGHS‐2 protein expression by ibuprofenoyl‐CoA thioesters.</jats:p></jats:list-item> <jats:list-item><jats:p>These data confirm that <jats:bold>S</jats:bold>‐ibuprofen represents the active entity in the racemate with respect to cyclo‐oxygenase activity. More importantly the data suggest a contribution of the <jats:bold>R</jats:bold>‐enantiomer to therapeutic effects not only by chiral inversion to <jats:bold>S</jats:bold>‐ibuprofen but also via inhibition of induction of PGHS‐2 mediated by <jats:bold>R</jats:bold>‐ibuprofenoyl‐CoA thioester.</jats:p></jats:list-item> <jats:list-item><jats:p>The data may explain why racemic ibuprofen is ranked as one of the safest non‐steroidal anti‐inflammatory drugs (NSAIDs) so far determined in epidemiological studies.</jats:p></jats:list-item> </jats:list> </jats:p><jats:p><jats:italic>British Journal of Pharmacology</jats:italic> (1997) <jats:bold>122</jats:bold>, 487–492; doi:<jats:ext-link xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" xlink:href="10.1038/sj.bjp.0701415">10.1038/sj.bjp.0701415</jats:ext-link></jats:p> Effects of ibuprofen enantiomers and its coenzyme A thioesters on human prostaglandin endoperoxide synthases British Journal of Pharmacology |
| spellingShingle | Neupert, Werner, Brugger, Roland, Euchenhofer, Christian, Brune, Kay, Geisslinger, Gerd, British Journal of Pharmacology, Effects of ibuprofen enantiomers and its coenzyme A thioesters on human prostaglandin endoperoxide synthases, Pharmacology |
| title | Effects of ibuprofen enantiomers and its coenzyme A thioesters on human prostaglandin endoperoxide synthases |
| title_full | Effects of ibuprofen enantiomers and its coenzyme A thioesters on human prostaglandin endoperoxide synthases |
| title_fullStr | Effects of ibuprofen enantiomers and its coenzyme A thioesters on human prostaglandin endoperoxide synthases |
| title_full_unstemmed | Effects of ibuprofen enantiomers and its coenzyme A thioesters on human prostaglandin endoperoxide synthases |
| title_short | Effects of ibuprofen enantiomers and its coenzyme A thioesters on human prostaglandin endoperoxide synthases |
| title_sort | effects of ibuprofen enantiomers and its coenzyme a thioesters on human prostaglandin endoperoxide synthases |
| title_unstemmed | Effects of ibuprofen enantiomers and its coenzyme A thioesters on human prostaglandin endoperoxide synthases |
| topic | Pharmacology |
| url | http://dx.doi.org/10.1038/sj.bjp.0701415 |