β-Amyrin ameliorates pulmonary fibrosis by inhibiting inflammatory response and oxidative stress in mice.

The study aimed to determine efficacy and mechanisms of β-Amyrin on pulmonary fibrosis. Use bleomycin (BLM) to induce the marine model of pulmonary fibrosis. β-Amyrin (20, 40, 80 mg/kg) was once treated via intragastrical administration for five consecutive days when after BLM stimulation. HE/Masson staining, hydroxyproline (HYP) content, Arterial blood gas analysis (BGA), inflammatory cytokines and oxidative stress factors were performed in this study. The lung gas-exchange function was significantly improved after being treated β-Amyrin with different concentrations, while IL-6, IL-1β, TNF-α and MCP-1 levels were decreased. And the increased fibrotic lesion in lung was also determined after treatment of β-Amyrin. Additionally, reduced MDA level and increase levels of GPX, SOD and GSH were also demonstrated using β-Amyrin in BLM-induced mice in a dose-dependent manner. In conclusions, our study determined that β-Amyrin has a potent efficacy in protecting against BLM-induced pulmonary fibrosis via suppressing inflammatory response and oxidative stress.