Further, ELISA results displayed that after overexpression of HDAC1 or silencing of PP2A in the PU-treated ALI mice, elevated levels of TNF-α, IL-1β, INF-γ, and IL-6 were observed (Fig. 5F), indicating that overexpressed HDAC1 or silenced PP2A curbed the alleviation of inflammatory responses by PU in the lung tissues of mice. This evidence concerns the gene IL1B and acute respiratory distress syndrome.