Abstract
Background Asthma is a complex inflammatory disorder that plagues a large number of people. Schisandrin B is an active ingredient of the traditional Chinese herbal medicine Schisandra with various proven physiological activities such as anti-inflammatory and antioxidant activities. In this study, we explored the anti-inflammatory and antioxidant effects and provided the mechanistic insights into the activity of schisandrin B in a mouse model of ovalbumin- (OVA-) induced allergic asthma. Methods Male BALB/c mice were sensitized and challenged with OVA to induce asthma and treated with various doses (15 mg/kg, 30 mg/kg, and 60 mg/kg) of SCH to alleviate the features of allergic asthma, airway hyperresponsiveness, inflammatory response, OVA-specific immunoglobulin (Ig)E level, and pathological injury. Results Schisandrin B significantly attenuated the airway hyperresponsiveness induced by OVA. Moreover, schisandrin B administration suppressed inflammatory responses, reduced the level of IgE, and attenuated pathological injury. Mechanistically, schisandrin B treatment promoted the activation of nuclear erythroid 2-related factor 2 (Nrf2), but suppressed the stimulation of the NF-κB pathway caused by OVA. Conclusion Taken together, our study suggests that schisandrin B attenuates the features of asthmatic lungs by inhibiting the NF-κB pathway and activating the Nrf2 signaling pathway.
Highlights
Asthma is a chronic and complicated airway disease that has become a global health problem in recent years
Interleukin-4 (IL-4), IL-13, and IL-5 are type 2 (Th2) cytokines that support the vital role of Th2 lymphocytes in asthma pathogenesis by reducing the release of immunoglobulin (Ig)E and eosinophil infiltration into lung tissues, which accelerate the process of allergic asthma [4, 5]
Airway reactivity is evaluated by calculating the percentage of Cdyn [14], which is interpreted as the change in lung volume in response to pressure, and RL, which is the compression force driving breathing divided by flow [13]
Summary
Asthma is a chronic and complicated airway disease that has become a global health problem in recent years. A large number of signaling pathways are involved in the pathophysiology of asthma Both nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) and nuclear erythroid 2-related factor 2 (Nrf2) pathways are strongly linked to airway inflammation and remodeling in asthma [7]. Specific activation of the Nrf pathway enhances the inhibition of the airway inflammatory response. Male BALB/c mice were sensitized and challenged with OVA to induce asthma and treated with various doses (15 mg/kg, 30 mg/kg, and 60 mg/kg) of SCH to alleviate the features of allergic asthma, airway hyperresponsiveness, inflammatory response, OVA-specific immunoglobulin (Ig)E level, and pathological injury. Schisandrin B treatment promoted the activation of nuclear erythroid 2-related factor 2 (Nrf2), but suppressed the stimulation of the NF-κB pathway caused by OVA. Our study suggests that schisandrin B attenuates the features of asthmatic lungs by inhibiting the NF-κB pathway and activating the Nrf signaling pathway
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