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http://dx.doi.org/10.15616/BSL.2018.24.2.102

Cardamonin Inhibits the Expression of Inducible Nitric Oxide Synthase Induced by TLR2, 4, and 6 Agonists  

Kim, Ah-Yeon (Department of Biomedical Laboratory Science, College of Medical Sciences, SoonChunHyang University)
Shim, Hyun-Jin (Department of Biomedical Laboratory Science, College of Medical Sciences, SoonChunHyang University)
Kim, Su-Yeon (Department of Biomedical Laboratory Science, College of Medical Sciences, SoonChunHyang University)
Heo, Sung-Hye (Department of Biomedical Laboratory Science, College of Medical Sciences, SoonChunHyang University)
Youn, Hyung-Sun (Department of Biomedical Laboratory Science, College of Medical Sciences, SoonChunHyang University)
Abstract
Toll-like receptors (TLRs) play an important role for host defense against invading pathogens. The activation of TLRs signaling leads to the activation of $NF-{\kappa}B$ and the expression of pro-inflammatory gene products such as cytokines and inducible nitric oxide synthase (iNOS). To evaluate the therapeutic potential of cardamonin, which is a naturally occurring chalcone from Alpinia species (zingiberaceous plant species), $NF-{\kappa}B$ activation and iNOS expression induced by MALP-2 (TLR2 and TLR6 agonist) or LPS (TLR4 agonist) were examined. Cardamonin inhibited the activation of $NF-{\kappa}B$ induced by MALP-2 or LPS. Cardamonin also suppressed the iNOS expression induced by MALP-2 or LPS. These results suggest that cardamonin has the specific mechanism for anti-inflammatory responses by regulating of TLRs signaling pathway.
Keywords
Cardamonin; Inducible nitric oxide synthase; TLR; Inflammation; LPS;
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