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Drug-Target Interaction

Drug

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PubChem ID:2214
Structure:
Synonyms:
1-(4-hydroxy-3-methoxyphenyl)-ethanone
1-(4-hydroxy-3-methoxyphenyl)ethan-1-one
1-(4-Hydroxy-3-methoxyphenyl)ethanone
3-Methoxy-4-hydroxyacetophenone
3-Metoksy-4-hydroksyacetofenon
3-Metoksy-4-hydroksyacetofenon [Polish]
4'-Hydroxy-3'-methoxyacetophenone
4-08-00-01814 (Beilstein Handbook Reference)
4-Acetyl-2-methoxyphenol
4-Hydroxy-3-methoxyacetophenone
4-Hydroxy-3-methoxyphenyl methyl ketone
498-02-2
A10809_ALDRICH
AA-504/20839006
AB1003774
AC-11656
AC1L1D6F
AC1Q46A5
AC1Q7AD6
Acetoguaiacon
Acetoguaiacone
Acetophenone, 4'-hydroxy-3'-methoxy-
ACETOPHENONE,4-HYDROXY,3-METHOXY ACETOVANILLON
ACETOPHENONE,4-HYDROXY,3-METHOXY ACETOVANILLON
Acetovanillon
Acetovanillone
Acetovanilone
Acetovanyllon
AI3-15892
AKOS000120562
Apocynin
Apocynine
AR-1H7512
BB_NC-2250
bmse000584
bmse010031
BRN 0637373
C056165
C11380
C9H10O3
CCRIS 7285
CHEBI:2781
CHEMBL346919
EINECS 207-854-5
Ethanone, 1-(4-hydroxy-3-methoxyphenyl)-
H0261
I01-7005
LS-13569
MLS001304972
MolPort-000-000-274
NCGC00247065-01
nchembio.83-comp20
NSC 209524
NSC209524
NSC2146
SBB008060
SMR000752909
W508454_ALDRICH
WLN: 1VR DQ CO1
ZINC00162515

Target

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Uniprot ID:NOS3_RAT
Synonyms:
cNOS
Constitutive NOS
EC-NOS
Endothelial NOS
eNOS
Nitric oxide synthase, endothelial
NOS type III
NOSIII
EC-Numbers:1.14.13.39
Organism:Rat
Rattus norvegicus
PDB IDs:-

Binding Affinities:

Ki: Kd:Ic 50:Ec50/Ic50:
----

References:

18001708
Inhibition of NADPH oxidase by apocynin inhibits lipopolysaccharide (LPS) induced up-regulation of arginase in rat alveolar macrophages.. Sonja Matthiesen; Dirk Lindemann; Mareille Warnken; Uwe R Juergens; Kurt Rack (2008) European journal of pharmacology display abstract
Reactive oxygen species participate in the pathogenesis of inflammatory airway diseases, in which increased arginase may play a role by interfering with nitric oxide (NO) synthesis and providing substrate for collagen synthesis. Therefore a modulatory role of reactive oxygen species for arginase was explored in alveolar macrophages using the NADPH oxidase inhibitor apocynin. The effects of lipopolysacharides (LPS) and apocynin on nitrite accumulation, arginase activity and mRNA for inducible NO synthase (iNOS), arginase I and II were determined. Superoxide anion (O(2)(-)) release was analysed by the iodonitrotetrazolium (INT) formazan assay. LPS (1 microg/ml) caused a 55%, transient increase in INT formation, i.e. O(2)(-) release which was inhibited by apocynin (500 microM). LPS caused a 2 fold increase in arginase activity and a marked increase in mRNA encoding arginase I, the predominant isoenzyme. Both effects were largely attenuated by apocynin. Apocynin did not affect the stability of arginase I mRNA, but accelerated the decline of arginase activity when protein synthesis was inhibited by cycloheximide. Apocynin also reduced LPS-induced nitrite accumulation (by 30%) and iNOS mRNA expression, but the magnitude of these effects was smaller than that on arginase I. Arginase I mRNA was also increased following exposure to hydrogen peroxide (H(2)O(2), 200 muM). In conclusion, inhibition of NADPH oxidase in alveolar macrophages causes down-regulation of arginase, indicating that reactive oxygen species exert stimulatory effects on arginase. Enhanced transcription of arginase mRNA and prolongation of the life time of the active enzyme appear to contribute to the enhanced arginase activity.