Allergic asthma is a chronic inflammatory disease that is regulated by coordination of T‑helper type 2 cell cytokines and inflammatory signaling molecules. Ginsenoside Rh2 (G‑Rh2) is an active component of ginseng with anti‑inflammatory and anti‑tumor effects. The aim of the present study was to determine the inhibitory effects of G‑Rh2 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 interleukin‑4 (IL‑4), IL‑5 and IL‑13; 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 (NF‑κB) in lung tissue. In the asthmatic mice, administration of G‑Rh2 markedly reduced peribronchiolar inflammation, recruitment of airway inflammatory cells, cytokine production, total and OVA‑specific IgE levels and AHR. G‑Rh2 administration inhibited NF‑κB activation and p38 mitogen-activated protein kinase (MAPK) phosphorylation induced by OVA inhalation. These results suggested that G‑Rh2 attenuates allergic airway inflammation by regulating NF‑κB activation and p38 MAPK phosphorylation. The present study identified the molecular mechanisms of action of G-Rh2, which supported the potential use of G‑Rh2 to prevent and/or treat asthma and other airway inflammatory disorders.

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