Mulberroside A ameliorates murine allergic airway inflammation by suppressing Th2 response and oxidative stress.

Mulberroside A is isolated from mulberries (Morus alba L.) and is reported to have anti-inflammatory responses in interleukin-1β-induced chondrocytes. However, the effects of mulberroside A on airway inflammation and airway hyperresponsiveness in asthmatic mice have not been reported. This study explored whether mulberroside A ameliorates airway inflammation and airway hyperresponsiveness in asthmatic mice. We also assessed the anti-inflammatory and antioxidant effects of mulberroside A in tracheal epithelial cells. We conducted a preclinical study using mouse models of induced asthma treated with mulberroside A and a complementary in vitro study using tracheal epithelial cells. Ovalbumin (OVA) or OVA/lipopolysaccharide (LPS)-sensitized female BALB/c mice were treated with an intraperitoneal injection of mulberroside A (10 mg/kg or 20 mg/kg). In the OVA-sensitized mouse model, mulberroside A attenuated airway hyperresponsiveness, inflammatory cell infiltration, and goblet cell hyperplasia in the lungs. Furthermore, it alleviated oxidative stress and airway inflammation by inhibiting Th2-associated cytokine expression. Treatment of inflammatory tracheal epithelial cells with mulberroside A effectively reduced the production of reactive oxygen species, pro-inflammatory cytokines, and eotaxin. Mulberroside A also inhibited monocyte attachment to inflammatory tracheal epithelial cells and reduced the levels of intercellular adhesion molecule-1. In the OVA/LPS-sensitized mouse model, mulberroside A significantly decreased neutrophil infiltration of lung tissue and bronchoalveolar lavage fluid, where it also inhibited some inflammatory cytokines and Th2-related cytokines. Thus, mulberroside A shows potential for improving airway inflammation in asthma.