[Formula: see text], a Rare Protopanaxatriol-Type Ginsenoside Fraction from Black Ginseng, Suppresses Inflammatory Gene iNOS via the Iinhibition of p-STAT-1 and NF-[Formula: see text]B.

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  • Additional Information
    • Source:
      Publisher: World Scientific Pub Country of Publication: Singapore NLM ID: 7901431 Publication Model: Print Cited Medium: Internet ISSN: 1793-6853 (Electronic) Linking ISSN: 0192415X NLM ISO Abbreviation: Am J Chin Med Subsets: MEDLINE
    • Publication Information:
      Publication: <2003->: Singapore ; River Edge, NJ : World Scientific Pub.
      Original Publication: [Garden City, N.Y.] : Institute for Advanced Research in Asian Science and Medicine
    • Subject Terms:
      Gene Expression/*drug effects ; Ginsenosides/*pharmacology ; Inflammation/*genetics ; NF-kappa B/*metabolism ; Nitric Oxide Synthase Type II/*genetics ; Nitric Oxide Synthase Type II/*metabolism ; Panax/*chemistry ; STAT1 Transcription Factor/*metabolism; Animals ; Anti-Inflammatory Agents ; Cyclooxygenase 2/genetics ; Cyclooxygenase 2/metabolism ; Ginsenosides/isolation & purification ; Heme Oxygenase-1/metabolism ; Human Umbilical Vein Endothelial Cells ; Humans ; Inflammation/drug therapy ; Inflammation Mediators/metabolism ; Interleukin-1beta/metabolism ; Luciferases/metabolism ; Male ; Mice, Inbred C57BL ; Phosphorylation/drug effects ; Phytotherapy
    • Abstract:
      Black ginseng (BG), which is ginseng that has been steamed and dried nine times, and its main protopanaxatriol-type ginsenosides Rg4, Rg6, Rh4, and Rg2 have been reported to exhibit various forms of biological activity, including antiseptic, antidiabetic, wound-healing, immune-stimulatory, and anti-oxidant activity. The aim of the this study was to examine the effects of [Formula: see text] (a rare protopanaxatriol-type ginsenoside fraction; Rg2, Rg4, Rg6, Rh1, and Rh4) on heme oxygenase-1 (HO-1) induction and on the expression of inducible nitric oxide synthase (iNOS) and cyclooxygenase (COX-)2 in lipopolysaccharide (LPS)-activated human pulmonary artery endothelial cells (HPAECs). [Formula: see text] was tested to determine its effect on iNOS protein expression and inflammatory markers (interleukin [IL]-1[Formula: see text] and tumor necrosis factor [TNF]-[Formula: see text] in the lung tissue of LPS-treated mice. The results showed that [Formula: see text] induced the expression of HO-1, reduced LPS-activated NF-[Formula: see text]B-luciferase activity, and inhibited iNOS/NO and COX-2/PGE2, which contributed to the inhibition of STAT-1 phosphorylation. In particular, [Formula: see text] induced the translocation of Nrf2 from the cytosol to the nucleus by increasing Nrf2-ARE activity and decreased IL-1[Formula: see text] production in LPS-activated HPAECs. This reduction in iNOS/NO expression due to [Formula: see text] was reversed by siHO-1 RNA transfection. In LPS-treated mice, [Formula: see text] significantly reduced lung tissue iNOS protein levels and TNF-[Formula: see text] levels in the bronchoalveolar lavage fluid. In conclusion, these findings indicate that [Formula: see text] has a critical anti-inflammatory effect due to its ability to regulate iNOS via the inhibition of p-STAT-1 and NF-[Formula: see text]B, and thus it may be suitable for the treatment of inflammatory disease.
    • Contributed Indexing:
      Keywords: Endothelium; [Formula: see text]; iNOS; p-STAT-1
    • Accession Number:
      0 (Anti-Inflammatory Agents)
      0 (Ginsenosides)
      0 (Inflammation Mediators)
      0 (Interleukin-1beta)
      0 (NF-kappa B)
      0 (STAT1 Transcription Factor)
      0 (STAT1 protein, human)
      EC 1.13.12.- (Luciferases)
      EC 1.14.13.39 (Nitric Oxide Synthase Type II)
      EC 1.14.14.18 (Heme Oxygenase-1)
      EC 1.14.99.1 (Cyclooxygenase 2)
    • Publication Date:
      Date Created: 20200717 Date Completed: 20201020 Latest Revision: 20201020
    • Publication Date:
      20231215
    • Accession Number:
      10.1142/S0192415X20500536
    • Accession Number:
      32668967