Jin Hur
Wonkwang University
5 Papers
12 Citations
Jin Hur is an academic researcher from Wonkwang University. The author has contributed to research in topics: Nitric oxide synthase & Nitric oxide. The author has an hindex of 5, co-authored 5 publications.
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Papers
KB-34, a newly synthesized chalcone derivative, inhibits lipopolysaccharide-stimulated nitric oxide production in RAW 264.7 macrophages via heme oxygenase-1 induction and blockade of activator protein-1
TL;DR: KB-34 suppresses NO production in LPS-stimulated RAW 264.7 macrophages via simultaneous induction of HO-1 expression and blockade of AP-1 activation, and reveals that KB-34 would be a promising agent for the treatment of inflammation-associated disease.
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Involvement of heme oxygenase-1 induction in inhibitory effect of ethyl gallate isolated from Galla Rhois on nitric oxide production in RAW 264.7 macrophages.
TL;DR: Results indicate that EG isolated from Galla Rhois suppresses NO production in LPS-stimulated RAW 264.7 macrophages via HO-1 induction, suggesting thatHO-1 is, at least in part, implicated in the inhibition of NO production induced by EG treatment.
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YL-I-108, a synthetic chalcone derivative, inhibits lipopolysaccharide-stimulated nitric oxide production in RAW 264.7 murine macrophages: Involvement of heme oxygenase-1 induction and blockade of activator protein-1
TL;DR: Results indicate that YL-I-108 suppresses NO production in LPS-stimulated macrophages via simultaneous induction of HO-1 expression and blockade of AP-1 activation.
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Inhibition of Nitric Oxide Production by Ethyl Digallates Isolated from Galla Rhois in RAW 264.7 Macrophages
TL;DR: Results indicate that EDG isolated from Galla Rhois suppresses LPS-stimulated NO production in RAW 264.7 macrophages via HO-1 induction.
2'-Methoxy-4'6'-bis(methoxymethoxy)chalcone inhibits nitric oxide production in lipopolysaccharide-stimulated RAW 264.7 macrophages.
TL;DR: 2'-methoxy-4'6'-bis(methoxymethoxy)chalcone (MBMC) inhibits LPS-stimulated nitric oxide production via down-regulation of inflammatory pathways (NF-kappaB, p38 and JNK) and induction of the protective enzyme, HO-1.
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