Atractylodin ameliorates bleomycin-induced pulmonary inflammation and fibrosis in mice

Abstract

IntroductionIdiopathic pulmonary fibrosis (IPF) is a chronic, progressive disease. The commonly used drugs for the treatment of pulmonary fibrosis can only delay the damage of lung function but cannot prolong the life of patients. Atractylodin (ATR), a kind of herbal medicine that has been proven to protect anti-inflammation and attenuate acute lung injury, was investigated to determine whether it could provide a new idea for the treatment of IPF by reducing the inflammatory reaction and collagen formation in the process of pulmonary fibrosis. MethodsIn vivo experiments, mice were divided into 6 groups, normal group, model, drug group (10 mg/kg, 30 mg/kg, 90 mg/kg) and positive control group (pirfenidone). Mice were given BLM through trachea, and after 24 h, normal saline, different concentrations of atractylodin and pirfenidone were given respectively. On 7 days, 14 days and 21 days, the weight, lung function, alveolar lavage fluid and lung tissue were tested. In vitro experiments to investigate the effect of atractylodin on fibroses, NIH3T3 cells were induced by TGF-β1 to detect the formation of cellular collagen and the phosphorylation level of Smad2/3 at different time points after their fibrosis. ResultsThe results showed that atractylodin could alleviate the lung function damage (FVC, FEV100, Tidal volume, tissue elastance) caused by BLM, reduce the inflammatory factors (IL-1β, IL-6, TNF-α), neutrophils and macrophage infiltration in the alveolar lavage fluid, as well as the formation and deposition of collagen (fibronectin, α-SMA, ColA1). In vitro studies have demonstrated that atractylodin can alleviate TGF-β1-induced pulmonary fibrosis by inhibiting the TGF-β1/Smad2/3 pathway. ConclusionAtractylodin can alleviate the lung function damage and attenuate pulmonary fibrosis induced by BLM through inhibiting the TGF-β1/Smad2/3 pathway. This may provide new ideas for the treatment of IPF.