Department of Respiration, Tangdu Hospital, The Fourth Military Medical University, Xi'an, Shaanxi 710038, P.R. China.
School of Accounting, Xijing University, Xi'an, Shaanxi 710032, P.R. China.
Int J Mol Med. 2018 Jun;41(6):3493-3500. doi: 10.3892/ijmm.2018.3528. Epub 2018 Mar 1.
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.
评价了 3,5,4'-三-O-乙酰白藜芦醇（AC-Res）通过干扰硫氧还蛋白-1（Trx-1）通路的激活对海水吸入性急性呼吸窘迫综合征（ARDS）的保护作用。通过肺水肿和肺炎症的严重程度评估海水吸入性 ARDS。通过 T-SOD 活性和肺及细胞中的 MDA 含量测试氧化应激。此外，还测量了 Trx-1、核因子红细胞 2 相关因子 2（Nrf2）和 Txnip 的表达，以探讨海水如何诱导氧化应激以及 AC-Res 减轻海水吸入性 ARDS 的机制。结果表明，海水吸入增加了肺组织的湿重/干重（W/D）比值，增强了肿瘤坏死因子-α（TNF-α）和白细胞介素-1β（IL-1β）的分泌，并通过干扰 Trx-1 通路扰乱了氧化应激平衡。而体内给予 AC-Res 和体外给予 Res 治疗可降低肺组织的 W/D 比值，减少肺部细胞因子，并通过 Trx-1 通路维持氧化应激平衡。总之，AC-Res 通过 Trx-1 通路减轻了海水吸入诱导的 ARDS。
