Allicin reduces airway inflammation and remodeling in a murine asthmatic model

Asthma is a complicated illness characterized by airway inflammation and tissue remodeling. Allicin, a naturally occurring sulfoxide, has been shown to possess a wide range of bioactive properties, including anti-inflammatory, antioxidative, and antitumor effects. This study primarily explores the role of allicin in airway inflammation and remodeling in a murine model of asthma. Mice were treated with varying doses (10 and 20 mg/kg) of allicin via intraperitoneal injection in an ovalbumin (OVA)-induced asthma model. The research team systematically evaluated the histopathological changes in the lung tissues and the changes in bronchoalveolar lavage fluid (BALF). The experimental results showed that allicin treatment significantly reduced OVA-triggered inflammatory cell infiltration and decreased the secretion of IL-4, IL-5, and IL-13 in BALF. Allicin notably alleviated OVA-induced thickening of smooth muscle and basement membranes, collagen deposition, as well as the expression of Collagen-Ⅰ and alpha-smooth muscle actin (α-SMA). Additionally, allicin administration reduced the expression of Phosphorylated Signal Transducer and Activator of Transcription 3 (p-STAT3) and PIM1 induced by OVA. Further in vitro experiments showed that allicin inhibits TGF-β1-induced cell proliferation in a dose-dependent manner. This inhibitory effect is associated with the suppression of STAT3 phosphorylation and PIM1 expression. The STAT3 agonist Colivelin reverses the anti-proliferative effects of allicin, while the inhibitor WP1066 enhances these effects. These findings collectively suggest that allicin exerts its anti-inflammatory and anti-remodeling effects in asthma by targeting the STAT3/PIM1 pathway, providing a new therapeutic strategy for asthma treatment.