Inhibitory Effects of Nardostachin on Nitric Oxide, Prostaglandin E2, and Tumor Necrosis Factor-α Production in Lipopolysaccharide Activated Macrophages

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  • Ju Hye Kyung
    College of Pharmacy, Yeungnam University
  • Baek Suk-Hwan
    Department of Biochemistry and Molecular Biology, College of Medicine, Yeungnam University
  • An Ren-Bo
    College of Pharmacy, Chungnam National University, Korea
  • Bae KiHwan
    College of Pharmacy, Chungnam National University, Korea
  • Son Kun Ho
    Department of Food and Nutrition, Andong National University, Korea
  • Kim Hyun Pyo
    College of Pharmacy, Kangwon National University, Korea
  • Kang Sam Sik
    Natural Products Research Institute, Seoul National University, Korea
  • Lee Sung Ho
    College of Pharmacy, Yeungnam University
  • Son Jong Keun
    College of Pharmacy, Yeungnam University
  • Chang Hyeun Wook
    College of Pharmacy, Yeungnam University

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タイトル別名
  • Inhibitory Effects of Nardostachin on Nitric Oxide, Prostaglandin E2, and Tumor Necrosis Factor-.ALPHA. Production in Lipopolysaccharide Activated Macrophages
  • Inhibitory Effects of Nardostachin on Nitric Oxide Prostaglandin E2 and Tumor Necrosis Factor アルファ Production in Lipopolysaccharide Activated Macrophages

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説明

Nardostachin, which is an iridoid isolated from Patrinia saniculaefolia, was examined by assessing its effect on the production of tumor necrosis factor-α (TNF-α) and expression of 2 enzymes, inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2), in lipopolysaccharide (LPS)-stimulated Raw264.7 macrophages. This compound consistently inhibited the production of nitric oxide (NO) and TNF-α production in a dose-dependent manner, with respective IC50 values of 12.3 and 16.2 μM. The decrease in quantity of NO products was accompanied by a decrease in the iNOS protein level, as assessed by Western blotting probed with specific anti-iNOS antibodies. In addition, this compound also reduced the COX-2 protein expression level and the attendant PGE2 production in LPS-stimulated macrophages. These results suggest that nardostachin may be useful for inhibiting the production of inflammatory mediators such as TNF-α, NO and PGE2 in inflammatory diseases.

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