Chikusetsusaponin IVa Methyl Ester Isolated from the Roots of Achyranthes japonica Suppresses LPS-Induced iNOS, TNF-α, IL-6, and IL-1β Expression by NF-κB and AP-1 Inactivation

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  • Lee Hae-Jun
    Department of Pharmaceutical Biochemistry, College of Pharmacy, Kyung Hee University Department of Life and Nanopharmaceutical Science, College of Pharmacy, Kyung Hee University
  • Shin Ji-Sun
    Department of Pharmaceutical Biochemistry, College of Pharmacy, Kyung Hee University Reactive Oxygen Species Medical Research Center, School of Medicine Kyung Hee University
  • Lee Woo-Seok
    Department of Pharmaceutical Biochemistry, College of Pharmacy, Kyung Hee University Department of Life and Nanopharmaceutical Science, College of Pharmacy, Kyung Hee University
  • Shim Heon-Yong
    Department of Pharmaceutical Biochemistry, College of Pharmacy, Kyung Hee University
  • Park Ji-min
    Department of Pharmaceutical Biochemistry, College of Pharmacy, Kyung Hee University Department of Life and Nanopharmaceutical Science, College of Pharmacy, Kyung Hee University
  • Jang Dae-Sik
    Department of Life and Nanopharmaceutical Science, College of Pharmacy, Kyung Hee University
  • Lee Kyung-Tae
    Department of Pharmaceutical Biochemistry, College of Pharmacy, Kyung Hee University Department of Life and Nanopharmaceutical Science, College of Pharmacy, Kyung Hee University

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  • Chikusetsusaponin IVa Methyl Ester Isolated from the Roots of <i>Achyranthes japonica</i> Suppresses LPS-Induced iNOS, TNF-α, IL-6, and IL-1β Expression by NF-κB and AP-1 Inactivation

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We investigated the effect of chikusetsusaponin IVa (CS) and chikusetsusaponin IVa methyl ester (CS-ME) from the roots of Achyranthes japonica NAKAI on lipopolysaccharide (LPS)-induced nitric oxide (NO) and prostaglandin E2 (PGE2) production in RAW264.7 macrophages. CS-ME more potently inhibited LPS-induced NO and PGE2 production than CS. CS-ME concentration-dependently inhibited LPS-induced tumor necrosis factor (TNF)-α and interleukin (IL)-6 and IL-1β production in RAW264.7 macrophages and mouse peritoneal macrophages. Consistent with these findings, CS-ME suppressed LPS-induced expression of inducible NO synthase (iNOS) and cyclooxygenase (COX)-2 at protein level as well as iNOS, COX-2, TNF-α, IL-6, and IL-1β at mRNA level. In addition, CS-ME suppressed LPS-induced transcriptional activity of nuclear factor (NF)-κB and activator protein (AP)-1. The anti-inflammatory properties of CS-ME might result from suppression of iNOS, COX-2, TNF-α, IL-6, and IL-1β expression through downregulation of NF-κB and AP-1 in macrophages.

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