Polysaccharide SAFP from Sarcodon aspratus attenuates oxidative stress-induced cell damage and bleomycin-induced pulmonary fibrosis.

Sarcodon aspratus, a popular edible fungus for its tasty flavour and can be used as a dietary supplement for its functional substances. Our study is conducted to evaluate the protective effect of Sarcodon aspratus polysaccharides (SAFP) on oxidative stress damage and pulmonary fibrosis (PF), and further explore the signaling pathways in vitro and in vivo. Results indicated that SAFP could enhance the A549 cells viability, prevent cell apoptosis and inhibit HO induced oxidative damage via attenuation of MDA and ROS levels. SAFP could also activate Nrf2 by inducing the translocation of Nrf2 from cytoplasm to nucleus as well as the level of HO-1. Pretreatment with SAFP could reduce bleomycin-induced pathological changes and collagen deposition in mice. Furthermore, SAFP could significantly upregulate antioxidase activities and downregulate fibrosis-associated indices including marker proteins, proinflammatory cytokines and profibrogenic cytokines. These findings indicated that SAFP could effectively attenuate HO-induced cellular oxidative stress through Nrf2/MAPK signaling pathway and delay progression of PF by reducing oxidative damage and inflammation through NF-κB/TGF-β1/MAPK pathway. Therefore, SAFP could be explored as a natural potential candidate drug for pulmonary fibrosis and other fibrosis-related diseases.