Gallic acid alleviates airway inflammation induced by cigarette smoke in mice

Abstract

Objective To investigate the effect of gllic acid (GA) on the pulmonary inflammatory response associated with chronic obstructive pulmonary disease (COPD) induced by cigarette smoking (CS) in mice. Methods The mouse model induced by CS was constructed. The counting number of inflammatory cells and the level of proinflammatory cytokines in bronchoalveolar lavage fluid were analyzed. The ROS, GSH, MDA and protein carbonyl activity in lung tissue homogenate were determined by commercially available kits. Western blot was used to analyze IL-13/STAT6 pathway. Results GA inhibited SC-induced inflammatory cell infiltration (neutrophils, lymphocytes, and macrophages) and decreased the level of pro-inflammatory cytokines (IL-6, TNF-α, and IL-1β). GA alleviated the redox imbalance and CS-induced airway inflammation in lung tissue of CS exposed mice. The later might be mediated by by inhibiting IL-13/STAT6 signaling pathway. Conclusions GA effectively modulates pulmonary inflammation and oxidative stress in mice associated with COPD pathogenesis.

Keywords

• gallic acid|il-13/stat6 signaling pathway|chronic obstructive pulmonary disease|airway inflammation