Background
DXM is widely used as an antifibrotic agent due to its protection of the lungs against fibrosis by inhibiting the production of inflammatory mediators. Many studies clearly indicated that the time point at which DXM treatment started, the dose and the duration of intervention are critical for exerting its antifibrotic effect. Exploring the role of DXM in the occurrence and development of PF at different stages is the fundamental
Conclusion
Long course of low-dose DXM intake following or after bleomycin administration both had therapeutic effects on pulmonary fibrosis.
Methods
Lung fibrosis was persuaded in Sprague-Dawley rats by a single intratracheal BLM (5 mg/kg) injection. This experiment was divided into two animal experiments and treated with DXM following or after bleomycin administration respectively. The biochemical, histopathological and molecular alterations were studied in the lung tissues.
Results
A long course of low-dose DXM had the ability to ameliorate PF induced by BLM via decreasing inflammation and improving oxidative stress through modulation of TGF-β/Smad, PI3K/Akt/mTOR and NF-κB signaling pathway.