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Sam Sik Kang

Researcher at Seoul National University

Publications -  275
Citations -  12207

Sam Sik Kang is an academic researcher from Seoul National University. The author has contributed to research in topics: Apoptosis & Oxidative stress. The author has an hindex of 59, co-authored 273 publications receiving 11086 citations. Previous affiliations of Sam Sik Kang include Chungnam National University & Kyung Hee University.

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Anti-inflammatory plant flavonoids and cellular action mechanisms.

TL;DR: The effect of flavonoids on eicosanoid and nitric oxide generating enzymes and the effect on expression of proinflammatory genes are summarized and a potential for new anti-inflammatory agents are discussed.
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Inhibition of inducible nitric oxide synthase and cyclooxygenase II by Platycodon grandiflorum saponins via suppression of nuclear factor-κB activation in RAW 264.7 cells

TL;DR: The results suggest that the main inhibitory mechanism of the platycodin saponins may be the reduction of iNOS and COX-2 gene expression through blocking of NF-κB activation.
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Effects of naturally occurring prenylated flavonoids on enzymes metabolizing arachidonic acid: Cyclooxygenases and lipoxygenases

TL;DR: In this article, the effects of 19 naturally occurring prenylated flavonoids, isolated from medicinal plants, on cyclooxygenase (COX)-1 and COX-2 and on 5-lipoxygenases (5-LOX) were investigated using [14C]arachidonic acid as a substrate.
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Anti-inflammatory effects of schisandrin isolated from the fruit of Schisandra chinensis Baill

TL;DR: In vitro results are the first that show that the anti-inflammatory properties of schisandrin result from the inhibition of nitric oxide production, prostaglandin E(2) (PGE(2)) release, cyclooxygenase-2 (COX-2) and inducible Nitric oxide synthase (iNOS) expression.
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Protective mechanism of glycyrrhizin on acute liver injury induced by carbon tetrachloride in mice.

TL;DR: It is suggested that glycyrrhizin alleviates CCl(4)-induced liver injury, and this protection is likely due to the induction of heme oxygenase-1 and the downregulation of proinflammatory mediators.