Ginsenoside Rh2 attenuates allergic airway inflammation by modulating nuclear factorκB activation in a murine model of asthma

Author:            

Publisher: Spandidos Publications

E-ISSN: 1791-3004|12|5|6946-6954

ISSN: 1791-2997

Source: Molecular Medicine Reports, Vol.12, Iss.5, 2015-01, pp. : 6946-6954

Disclaimer: Any content in publications that violate the sovereignty, the constitution or regulations of the PRC is not accepted or approved by CNPIEC.

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Abstract

Allergic asthma is a chronic inflammatory disease that is regulated by coordination of Thelper type 2 cell cytokines and inflammatory signaling molecules. Ginsenoside Rh2 (GRh2) is an active component of ginseng with antiinflammatory and antitumor effects. The aim of the present study was to determine the inhibitory effects of GRh2 on allergic airway inflammation in a murine model of asthma, in which mice develop the following pathophysiological features of asthma: Increased abundance of inflammatory cells; increased levels of interleukin4 (IL4), IL5 and IL13; decreased abundance of interferon gamma in the bronchoalveolar lavage fluid and lung tissue; increased total and ovalbumin (OVA)specific immunoglobulin E (IgE) levels in the serum; increased airway hyperresponsiveness (AHR); and activation of nuclear factor kappa B (NFκB) in lung tissue. In the asthmatic mice, administration of GRh2 markedly reduced peribronchiolar inflammation, recruitment of airway inflammatory cells, cytokine production, total and OVAspecific IgE levels and AHR. GRh2 administration inhibited NFκB activation and p38 mitogen-activated protein kinase (MAPK) phosphorylation induced by OVA inhalation. These results suggested that GRh2 attenuates allergic airway inflammation by regulating NFκB activation and p38 MAPK phosphorylation. The present study identified the molecular mechanisms of action of G-Rh2, which supported the potential use of GRh2 to prevent and/or treat asthma and other airway inflammatory disorders.