Arbutin Alleviates LPS Induced Sepsis Pneumonia in Mice

The aim of this study was to investigate the effects of arbutin (AR) on lipopolysaccharide (LPS)-induced sepsis pneumonia. LPS-induced mice and A549 cells were used to establish septic pneumonia model. AR significantly decreased lung wet-to-dry weight (W/D) ratio, lung myeloperoxidase (MPO) activity and ameliorated lung histopathological changes. In addition, AR increased super oxide dismutase (SOD) activity, decreased malondialdehyde (MDA) content and levels of cytokines including tumor necrosis factor-α (TNF-α), interleukin-1β (IL-β) and interleukin-6 (IL-6) in bronchoalveolar lavage fluid (BALF) in mice. Furthermore, the results demonstrated that AR inhibited the JAK2/STAT3/NF-κB pathway in LPS-induced A549 cells which was further confirmed by siRNA JAK2 experiment. The experimental results indicated that the protective mechanism of AR on sepsis pneumonia might be attributed partly to the inhibition of cytokine production and JAK2/STAT3/NF-κB pathway.