Protective effects of syringin against lipopolysaccharide-induced acute lung injury in mice.

Syringin, a major active substance isolated from Eleutherococcus senticosus, has been found to have anti-inflammatory effect. The aim of this study was to investigate the effects and underlying mechanisms of syringin on lipopolysaccharide (LPS)-induced acute lung injury (ALI) in mice.

We established an LPS-induced ALI model in mice. We also detected the lung wet-to-dry ratio, myeloperoxidase activity, and inflammatory cytokines tumor necrosis factor alpha, interleukin (IL)-1β, and IL-6 to estimate the index of lung injury in mice. Furthermore, the expression of nuclear factor-erythroid 2-related factor-2 (Nrf2), heme oxygenase-1, and nuclear factor κB (NF-κB) was detected by Western blot analysis.

The results showed that the increases in lung wet-to-dry ratio, myeloperoxidase activity, malondialdehyde content, and levels of tumor necrosis factor alpha, IL-1β, and IL-6 induced by LPS were significantly inhibited by treatment of syringin. The phosphorylation of IκB-α and p65 NF-κB caused by LPS was inhibited by syringin. Furthermore, syringin was found to upregulate the expression of Nrf2 and heme oxygenase 1.

In conclusion, the results suggest that syringin protects against LPS-induced ALI by activating Nrf2 and inhibiting NF-κB signaling pathway.