Abstract
Asthma affects a large number of people worldwide and is characterized by chronic allergic airway inflammation. Anatabine is a natural alkaloid that is structurally similar to nicotine and found in the Solanaceae family of plants, with anti-inflammatory properties. Consequently, this study aimed to evaluate the potential therapeutic effect of anatabine against asthma.
Ovalbumin was used to induce asthma in rats. Two asthmatic groups were treated with low and high doses of anatabine.
Asthmatic animals experienced increased total leukocyte count and inflammatory cytokines in bronchoalveolar lavage fluid (BALF), bronchitis, and bronchopneumonia associated with mast cell infiltration. Additionally, inducible nitric oxide synthase immunostaining was observed, with decreased pulmonary antioxidant capacity and enzymes and decreased Nrf2 and HO-1 gene expression while increased NFκB-P65 expression. Interestingly, asthmatic animals treated with anatabine at both doses showed dose-dependently decreased inflammatory cells and cytokine levels within BALF reduced inflammation in the airways through decreased mast cell infiltration within lung tissues and increased antioxidant enzymes and Nrf2 and Ho-1 expression levels.
Our results highlight the potential beneficial effect of anatabine against asthma through anti-inflammatory and antioxidant mechanisms. Therefore, anatabine is a promising candidate for pulmonary asthma treatment.
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•We conducted this study to evaluate the potential therapeutic effect of anatabine against asthma. Ovalbumin was used to induce asthma in rats. Two asthmatic groups were treated with low and high doses of anatabine.•OVA-challenged rats showed pulmonary lesions mimicking asthma that were associated with high serum IgE levels, increased inflammatory cytokines, and oxidative stress in the BALF, eosinophils, and mast cell tissue infiltration, and low pulmonary surfactants.•The administration of Anatabine markedly ameliorated OVA-induced asthma and obstructive lesions via mitigation of oxidative stress and inflammation, and upregulation of Nrf2/HO-1 signaling in rats.