Cinnamaldehyde modulates oxidative stress and NF-κB signaling in OVA-induced asthmatic BALB/c mice.

Abstract

Asthma remains a challenging condition with limited treatment options. Cinnamaldehyde (Cinn), a compound that is naturally recognized for its anti-inflammatory and antioxidant capabilities, has garnered considerable scientific interest. This study aims to evaluate the effects of low and high doses of Cinn compared to dexamethasone (Dexa), a conventional corticosteroid, in a murine model of ovalbumin (OVA)-induced asthma. Asthma was generated in BALB/c mice through OVA sensitization and challenge. The mice were categorized into five groups (n = 8): Control, OVA, Cinn (20mg/kg), Cinn (40mg/kg), and Dexa (1mg/kg). The investigation evaluated airway inflammation, histological alterations, and inflammatory biomarkers for a duration of 16 days. Treatments were administered orally from days 11 to 16. Cinn administration significantly reduced oxidative stress, as indicated by reduced levels of nitric oxide and malondialdehyde, while simultaneously boosting antioxidant defenses through elevated glutathione and catalase levels. The Cinn-treated groups exhibited a significant reduction in serum immunoglobulin E levels, serum interleukin-13 (IL-13), and immune cell infiltration in bronchoalveolar lavage fluid (BALF), as well as decreased peribronchial inflammation and goblet cell metaplasia in lung histology. Moreover, Cinn inhibited the expression of phosphor-nuclear factor kappa B (p-NFκB-p65) in lung tissues, resulting in decreased immune cell infiltration in BALF, as well as reduced peribronchial inflammation and goblet cell metaplasia. Both dosages of Cinn markedly reduced airway inflammation and histological changes relative to the OVA group, with results similar to those of Dexa, particularly at the higher dose. The data indicate that Cinn demonstrates significant anti-inflammatory and antioxidant properties, making it a promising candidate for the prevention and treatment of asthma.