Xueying Liu

The protecting effects of 3,5,4'-tri-O-acetylresveratrol (AC-Res) on seawater inhalation-induced acute respiratory distress syndrome (ARDS) by interfering with the activation of thioredoxin-1 (Trx-1) pathway were evaluated. Seawater inhalation-induced ARDS was assessed by magnitude of pulmonary edema and lung inflammation. Oxidative stress was tested by T-SOD activity and MDA content in lungs and cells. Besides, Trx-1, nuclear factor erythroid 2-related factor 2 (Nrf2) and Txnip expression were measured to explore how seawater induced oxidative stress and the mechanism by which AC-Res attenuated seawater inhalation-induced ARDS. The results showed that seawater inhalation increased wet-to-dry (W/D) ratios of lung tissues, enhanced secretion of tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β), and disturbed the oxidative distress balance probably through interfering the activity of Trx-1 pathway. While treatment of AC-Res in vivo and Res in vitro reduced W/D ratios of lung tissues, decreased cytokines in lungs and maintained the oxidative stress balance through Trx-1 pathway. In conclusion, AC-Res treatment attenuated seawater inhalation induced ARDS via Trx-1 pathway.

The aim of the present research was to investigate the protecting effects of 3,5,4′‐tri‐O‐acetylresveratrol (AC‐Rsv) on LPS‐induced acute respiratory distress syndrome (ARDS). Lung injuries have been evaluated by histological examination, wet‐to‐dry weight ratios, and cell count and protein content in bronchoalveolar lavage fluid. Inflammation was assessed by MPO activities and cytokine secretion in lungs and cells. The results showed that AC‐Rsv significantly reduced the mortality of mice stimulated with LPS. Pretreatment of AC‐Rsv attenuated LPS‐induced histological changes, alleviated pulmonary edema, reduced blood vascular leakage, and inhibited the MPO activities in lungs. What was more, AC‐Rsv and Rsv treatment reduced the secretion of TNF‐α, IL‐6, and IL‐1β in lungs and NR8383 cells, respectively. Further exploration revealed that AC‐Rsv and Rsv treatment relieved LPS‐induced inhibition on SIRT1 expression and restrained the activation effects of LPS on MAPKs and NF‐κB activation both in vitro and in vivo. More importantly, in vivo results have also demonstrated that the protecting effects of Rsv on LPS‐induced inflammation would be neutralized when SIRT1 was in‐hibited by EX527. Taken together, these results indicated that AC‐Rsv protected lung tissue against LPS‐induced ARDS by attenuating inflammation via p38 MAPK/SIRT1 pathway.