In this study, we investigated the effects of astragaloside IV (As-IV) on pulmonary fibrosis and its mechanisms of action. Sprague-Dawley rats were used in a model of pulmonary fibrosis induced by an intratracheal instillation of bleomycin (BLM). Rats were intraperitoneally injected with As-IV (10, 20, 50 mg/kg) daily for 28 days, while the rats in control and BLM groups were injected with a saline solution. The effects of As-IV treatment on pulmonary injury were evaluated with the lung wet/dry weight ratios, cell counts, and histopathologic. Oxidative stress was evaluated by detecting the levels of malondialdehyde (MDA), superoxide dismutase (SOD), total antioxidant capacity (T-AOC), and reactive oxygen species (ROS) in lung tissue. Inflammation was assessed by measuring the levels of tumor necrosis factor (TNF)-α, interleukin (IL)-1β, and IL-6 in bronchoalveolar lavage fluid (BALF). The results indicated that As-IV treatment remarkably ameliorated BLM-induced pulmonary fibrosis and attenuated BLM-induced oxidative stress and inflammation. Our findings indicate that As-IV-mediated suppression of fibroproliferation may contribute to the anti-fibrotic effect against BLM-induced pulmonary fibrosis. Its mechanisms of action are associated with inhibiting oxidative stress and inflammatory response. In summary, our study suggests a therapeutic potential of As-IV in the treatment of pulmonary fibrosis.

Not applicable.

Our study suggests that the NLRP3 SNP rs10754558 is associated with the incidence of AV. The G allele might be a genetic risk factor for AV in the Chinese population.