Melia azedarach L. reduces pulmonary inflammation and mucus hypersecretion on a murine model of ovalbumin exposed asthma

Abstract

Ethnopharmacological relevanceMelia azedarach L. is a traditional medicinal plant used to control pain, pyrexia, inflammation and bacterial infections that possesses several pharmacological activities, including anti-inflammatory and antioxidant activities. Particularly, the root of M. azedarach was used as expectorant and anti-cough and asthma treatment. Based its properties, M. azedarach is expected to have a potential to treat allergic asthma, chronic inflammatory respiratory disease. However, there is no study on anti-asthmatic effects of M. azedarach and its mechanism of action until now. Aim of the studyWe investigated the active ingredient of M. azedarach fruit extract (MAE) using high-performance liquid chromatography (HPLC) and explored the therapeutic effects of MAE on pulmonary inflammation and mucus hypersecretion using a murine model of ovalbumin (OVA) exposed asthma. Materials and methodsThe ingredients of MAE were analyzed using HPLC. To develop allergic asthma model, the animals were sensitized (days 1 and 14) and the airway was challenged (from day 21–23) using OVA. MAE was administered by oral gavage once a day from day 18–23 at doses of 30 and 100 mg/kg. ResultsHPLC analysis revealed the presence of toosendanin in MAE. In asthmatic mice, MAE administration effectively suppressed the inflammatory cell counts in bronchoalveolar lavage fluid (BALF) along with a reduction in airway hyperresponsiveness. Moreover, MAE administration inhibited the production of proinflammatory cytokines and immunoglobulin E in BALF and serum of asthmatic mice, respectively. These results were similar to the results of histological examination showing a reduction in pulmonary inflammation and mucus hypersecretion. MAE elevated the expression of nuclear factor erythroid 2-related factor 2, heme oxygenase-1, and superoxide dismutase 2, which in turn resulted in the suppression of matrix metallopeptidase-9 expression in lung tissue of asthmatic mice. ConclusionsAltogether, MAE successfully inhibited allergic asthma in OVA-exposed mice. Thus, MAE could be a potential therapeutic remedy for treating allergic asthma.