Wogonin Attenuates Bleomycin-Induced Pulmonary Fibrosis and Oxidative Stress Injury via the MAPK Signaling Pathway.

Idiopathic pulmonary fibrosis (PF) is an irreversible and chronic inflammatory condition with limited therapeutic options and a high mortality rate. We aimed to determine the possible role and mechanisms of wogonin (WGN) on PF. A rat model of PF was established with intratracheally administrated with bleomycin (BLM), followed by intravenously injecting with WGN and weekly body weight measurements for four weeks. Hematoxylin-eosin (H&E) and Masson's trichrome staining were implemented for histopathological analysis. In addition, the levels of fibrotic proteins and indicators of the mitogen-activated protein kinase (MAPK) pathway were assessed with Western blot. RT-quantitative (q)PCR experiment was conducted to investigate the fibrotic proteins' mRNA expression. Ultimately, the concentrations of glutathione peroxidase (GSH-PX), malonaldehyde (MDA), and superoxide dismutase (SOD) were ascertained with appropriate kits. The results showed that WGN administration significantly reversed BLM-induced body weight reduction, alleviated pathological fibrosis, and reduced the Ashcroft score and the lung wet-to-dry weight ratio. Additionally, WGN suppressed the rise of fibrotic protein levels in BLM-treated rat's lung tissues. Furthermore, WGN attenuated BLM-stimulated oxidative stress, as evidenced by the increased GSH-PX and SOD levels and decreased MDA levels in vivo. Finally, wogonin supplements significantly lowered the extracellular signal-regulated kinase (ERK), c-Jun N-terminal kinase (JNK), and p38 MAPK phosphorylation levels in the BLM-treated rat's lung tissues. In conclusion, our study proved that PF induced by BLM administration can be mitigated by WGN treatment via suppressing the MAPK pathway, indicating that WGN is a candidate therapeutic agent for managing PF.