Effects of Ampelopsis brevipedunculata on Ovalbumin-Induced Allergic Airway Inflammation via Regulating Mast Cell Activation and PLCγ/Akt/NF-κB Signaling Pathway

Asthma is a chronic allergic airway inflammation that requires ongoing therapeutic intervention and reduces the patient’s quality of life. Therefore, safe and efficacious drugs for the treatment of asthma are urgently needed. This study investigated whether the ethyl acetate fraction derived from a 95% (v/v) ethanol extract of dried Ampelopsis brevipedunculata (ABE) alleviates allergic airway inflammation. To investigate the anti-allergic and anti-inflammatory effects of ABE, a mouse model of ovalbumin (OVA)-induced allergic airway inflammation was used and clarified their mechanisms in mast cells. ABE administration reduced the asthmatic symptoms and levels of pro-inflammatory mediators and cytokines by 45–70% in bronchoalveolar lavage fluid (BALF) and by 55–80% in lung tissue compared with the OVA group. ABE administration decreased the levels of serum immunoglobulins (Igs) including IgG1, IgG2a, IgE, and OVA-specific IgE by 30–55% compared with the OVA group. In addition, ABE ameliorated mast cell infiltration and activation which reflected the degree of allergic airway inflammation in the lung and BALF. ABE inhibited mast cell degranulation, suppressing intracellular calcium influx by approximately 30% relative to the DNP-HSA group. It also prevented pro-inflammatory gene expression of mast cells by 35–70% relative to the DNP-HSA group through blocking the FcεRI-NF-κB signaling pathway. Moreover, the isolated compounds from ABE (syringic acid, ellagic acid, resveratrol, catechin, and 4′-O-(β-D-glucopyranosyl)-3,3′4-tri-O-methylellagic acid) inhibited mast cell degranulation and pro-inflammatory cytokine expression by suppressing the PLCγ, Akt, and NF-κB signaling pathways. Taken together, these findings suggest that ABE and its constituents are potential novel therapeutic agents for allergic airway inflammation.