Protective Effects of Polypodiside as a Nrf2 Activator on Beas-2B Cells Against the Injury Induced by LPS

. Acute lung injury (ALI) followed by acute respiratory distress syndrome (ARDS) are the lethal lung diseases. It was found activating Nrf2 could attenuate inflammation, oxidative stress and apoptosis in ALI/ARDS. To discover novel therapeutic for ALI/ARDS, polypodiside was explored using Beas-2B cells injured by LPS. The results showed polypodiside improved the viability of Beas-2B cells treated with LPS and suppressed oxidative stress via reducing ROS and MDA, and elevating SOD, CAT and GPx. Meanwhile, the inflammation resulting from LPS in Beas-2B cells was ameliorated by polypodiside through decreasing the pro-inflammatory cytokines including TNF-alpha IL-1 beta and IL-6. It was also found NF-kappa B was inactivated by polypodiside. In addition, polypodiside down-regulated caspase-3 and Bax and up-regulated Bcl-2 to inhibit apoptosis of Beas-2B cells induced by LPS. Then the activation of Nrf2 in Beas-2B cells was associated with the protective effects of polypodiside.