Dian sanguis draconis improves pulmonary fibrosis by activating autophagy to regulate the PA/PAI-1 balance.

Abstract

Background: Pulmonary fibrosis (PF) is a severe lung disease that manifests as lung tissue destruction and collagen deposition and easily leads to respiratory failure. It is difficult to reverse these conditions using current treatment methods. This study focused on the exploration and development of novel drugs for the treatment of PF.

Methods: This study simulated the pathological process of PF by using a bleomycin (BLM)-induced rat model and a TGF-β1-induced in vitro cell model. Dian sanguis draconis (DSD) was used for intervention, and the effects on the lung tissue structure, collagen fiber deposition, autophagy level and PA/PAI-1 balance were evaluated via pathological tissue staining, western blotting, and ELISA.

Results: In untreated PF rats, severely disordered lung tissue, thickened alveolar septa, and excessive deposition of collagen fibers were observed. In addition, the level of autophagy was inhibited, and the balance of PA/PAI-1 in the lung tissue was disrupted. After treatment with DSD, these pathological injuries improved, as demonstrated by the restoration of lung tissue structure, reduction in collagen fiber deposition, recovery of autophagy levels, and remodeling of the PA/PAI-1 balance. In addition, mechanistically, DSD improves PF by increasing the level of autophagy-related proteins and regulating the PA/PAI-1 balance.

Conclusion: This study confirmed the significant effect of DSD in alleviating PF. These findings provide new drug candidates for the treatment of PF.