Asthma comprises a triad of reversible
airway obstruction, bronchial smooth muscle cell hyperreactivity to
bronchoconstrictors, and chronic bronchial
inflammation. Clinical and experimental findings have established
eosinophilia as a sign of allergic disorders. In the present investigation, we evaluated the
anti-asthmatic effects of
schizandrin and its underlying mechanisms in an in vivo murine asthmatic model. To accomplish this, female BALB/c mice were sensitized and challenged with
ovalbumin (OVA), and examined for the following typical asthmatic reactions: increased numbers of eosinophils and other inflammatory cells in bronchoalveolar lavage fluid (BALF); production of Th1
cytokines (such as
tumor necrosis factor (TNF)-α in BALF); production of Th2
cytokines (such as
interleukin IL-4 and IL-5) in BALF; presence of total and OVA-specific
immunoglobulins (Ig)E in serum; presence of oxidative stress;
hyperplasia of goblet cells in the lung; and marked influx of inflammatory cells into the lung. Our results collectively show that
schizandrin exerts profound inhibitory effects on accumulation of eosinophils into the airways and reduces the levels of
IL-4,
IL-5, IFN-γ, and TNF-α in BALF. Additionally,
schizandrin suppresses the production of
reactive oxygen species (ROS) in a dose-dependent manner, and inhibits goblet cell
hyperplasia and inflammatory cell infiltration in lung tissue. Thus,
schizandrin has
anti-asthmatic effects, which seem to be partially mediated by reduction of oxidative stress and airway
inflammation, in a murine allergic
asthma model. These results indicate that
schizandrin may be an effective novel therapeutic agent for the treatment of allergic
asthma.