Alamandine reduces oxidative stress and preserves the epithelium in BLM-induced pulmonary fibrosis

Pulmonary Fibrosis (PF) is an interstitial lung disease in which healthy lung tissue is replaced by scar tissue, mainly composed of mesenchymal cells and extracellular matrix. Studies have demonstrated a crucial role for increased oxidative stress in PF pathogenesis and fibroblast recruitment. Recently, our group demonstrated that treatment with Alamandine (ALA) attenuates the clinical effects of PF in an experimental model. However, its effects on redox balance and pulmonary epithelial cellularity have not yet been investigated. Therefore, this study evaluated the antioxidant potential of ALA and fibroblast presence in the lungs of rats with induced PF and treated with ALA.

To induce PF, Bleomycin was administered to Wistar rats, and treatment with ALA began simultaneously. After 14 days, the animals were euthanized, and their lungs were collected for immunohistochemical and redox state analysis.

ALA reduced the number of mesenchymal cells (P < 0.0001), including myofibroblasts (P < 0.005). Additionally, ALA restored total glutathione levels (P < 0.0001) and antioxidant capacity (P < 0.005), while controlling advanced oxidation protein products (P < 0.05) and fluorescence intensity (P < 0.0001), maintaining values like those of the control group.

Our results showed that ALA helps maintain the pulmonary epithelium in a state close to healthy conditions in an experimental PF model. Additionally, we demonstrated that ALA exhibits antioxidant effects by controlling the production of reactive oxygen species. While further studies are warranted, our findings strongly suggest that ALA could be a promising therapeutic option for treating pulmonary fibrosis.