Rutaecarpine Attenuates Ovalbumin-Induced Asthma in Mice by Regulating the NF-κB Pathway.

Abstract

Pediatric asthma is a common chronic condition with several pathological features, including airway inflammation, remodeling, and oxidative stress. Rutaecarpine (RUT), a bioactive alkaloid, exhibits therapeutic efficacy against various allergic diseases. However, its roles in asthma and the underlying molecular mechanisms remain elusive. In this study, we established an ovalbumin (OVA)-induced mouse model of asthma. The results showed that compared with the OVA-challenged group, treatment with RUT (10 and 20 mg/kg) reduced lung tissue inflammatory scores by 37.5% and 50.0%, respectively. Additionally, RUT suppressed the production of interleukin (IL)-4, IL-5, and IL-13, and decreased the counts of total cells, eosinophils, macrophages, neutrophils, and lymphocytes in bronchoalveolar lavage fluid. Regarding airway remodeling, RUT downregulated the mRNA and protein expression of α-smooth muscle actin and type I collagen. Furthermore, periodic acid-Schiff staining showed that RUT ameliorated OVA-induced mucus hypersecretion. RUT treatment also exhibited a protective effect on OVA-induced oxidative damage in lung tissues. Mechanistically, RUT suppressed OVA-induced activation of the nuclear factor-kappa B (NF-κB) pathway. Collectively, RUT attenuated inflammation, airway remodeling, and oxidative stress in OVA-induced asthmatic mice by inhibiting the NF-κB pathway, highlighting its potential as an adjunct therapy for pediatric asthma and providing a theoretical basis for future clinical translation.