• Title/Summary/Keyword: Biochemistry

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The Anti-Inflammatory Effect of IH-901 in HT-29 Cells

  • Lee, Seung-Min;Kim, Ki-Nam;Kim, Yu-Ri;Kim, Hye-Won;Shim, Boo-Im;Lee, Seung-Ho;Bae, Hak-Soon;Kim, In-Kyoung;Kim, Meyoung-Kon
    • Molecular & Cellular Toxicology
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    • v.3 no.4
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    • pp.254-261
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    • 2007

  • 20-O-($\beta$-D-Glucopyranosyl)-20 (S)-protopanaxadiol (IH-901) is one of the major metabolites of ginsenosides from Panax ginseng, and is suggested that IH-901 has been associated with various pharmacological and physiological activities. In this study, we demonstrate that IH-901 induced anti-inflammation in HT-29 human colon adenocarcinoma cells. Our results showed that IH-901 inhibited cell proliferation of HT-29 in a time- and dose-dependent manner. We also found that IH-901 was significantly decreased expression of iNOS compared with non-treated. We observed effect of IH-901 related with inflammatory genes using by cDNA microarray. We were known that the 34 inflammatory genes such as E2F, CDK6, TNF-$\alpha$, and PKC were down-regulated. Thus, these results suggest that IH-901 may have a potential preventive factor to improving cancer induced by chronic inflammation.

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Heme oxygenase-1 (HO-1)/carbon monoxide (CO) axis suppresses RANKL-induced osteoclastic differentiation by inhibiting redox-sensitive NF-κB activation

  • Bak, Sun-Uk;Kim, Suji;Hwang, Hae-Jun;Yun, Jung-A;Kim, Wan-Sung;Won, Moo-Ho;Kim, Ji-Yoon;Ha, Kwon-Soo;Kwon, Young-Guen;Kim, Young-Myeong
    • BMB Reports
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    • v.50 no.2
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    • pp.103-108
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    • 2017

  • Heme oxygenase (HO-1) catalyzes heme to carbon monoxide (CO), biliverdin/bilirubin, and iron and is known to prevent the pathogenesis of several human diseases. We assessed the beneficial effect of heme degradation products on osteoclastogenesis induced by receptor activator of NF-${\kappa}B$ ligand (RANKL). Treatment of RAW264.7 cells with CORM-2 (a CO donor) and bilirubin, but not with iron, decreased RANKL-induced osteoclastogenesis, with CORM-2 having a more potent anti-osteogenic effect. CORM-2 also inhibited RANKL-induced osteoclastogenesis and osteoclastic resorption activity in marrow-derived macrophages. Treatment with hemin, a HO-1 inducer, strongly inhibited RANKL-induced osteoclastogenesis in wild-type macrophages, but was ineffective in $HO-1^{+/-}$ cells. CORM-2 reduced RANKL-induced NFATc1 expression by inhibiting IKK-dependent NF-${\kappa}B$ activation and reactive oxygen species production. These results suggest that CO potently inhibits RANKL-induced osteoclastogenesis by inhibiting redox-sensitive NF-${\kappa}B$-mediated NFATc1 expression. Our findings indicate that HO-1/CO can act as an anti-resorption agent and reduce bone loss by blocking osteoclast differentiation.

  • https://doi.org/10.5483/BMBRep.2017.50.2.220 인용 PDF KSCI