Cai Xuemei, Wu Yanan, Liu Fuxia, He Jinping, Bi Yanhua
Department of Pharmacy, Huabei Petroleum Administration Bureau General Hospital, Renqiu, Hebei Province 062550, China.
Department of Traditional Chinese Medicine, Huabei Petroleum Administration Bureau General Hospital, Renqiu, Hebei Province 062550, China.
Tissue Cell. 2025 Apr;93:102698. doi: 10.1016/j.tice.2024.102698. Epub 2024 Dec 24.
Acute lung injury (ALI) is the critical respiratory condition. Syringin with anti-inflammatory and anti-oxidant properties can exhibit the lung protective effects. SIRT1 and STAT6 can exert protective roles against lung injury by inhibiting ferroptosis.
In the current study, A549 lung epithelial cells were treated with 200 μM HO for 2 h to establish an in vitro ALI model. Then, HO-stimulated A549 cells were treated with syringin to identify the biological role of syringin in ROS-induced ALI. Moreover, HO-stimulated A549 cells were further treated with SIRT1 inhibitor EX527 or ferroptosis activator erastin to elucidate whether syringin could exert protective effects against ROS-induced ALI depending on SIRT1/STAT6 signaling-mediated ferroptosis inhibition.
It was verified that syringin treatment improved the impaired viability and mitigated inflammatory response and oxidative stress of HO-stimulated A549 lung epithelial cells by activating SIRT1/STAT6 signaling pathway. Syringin treatment inhibited the ferroptosis of HO-stimulated A549 lung epithelial cells by activating SIRT1/STAT6 signaling pathway. Treatment with SIRT1 inhibitor EX527 or ferroptosis activator erastin both reversed the alleviating effect of syringin on HO-induced A549 lung epithelial cell injury.
To sum up, syringin treatment alleviates HO-induced lung epithelial cell injury by activating SIRT1/STAT6 signaling pathway to inhibit ferroptosis.
急性肺损伤（ALI）是一种严重的呼吸系统疾病。具有抗炎和抗氧化特性的紫丁香苷可发挥肺保护作用。沉默调节蛋白1（SIRT1）和信号转导和转录激活因子6（STAT6）可通过抑制铁死亡对肺损伤发挥保护作用。
在本研究中，用200μM过氧化氢（HO）处理A549肺上皮细胞2小时以建立体外ALI模型。然后，用紫丁香苷处理HO刺激的A549细胞，以确定紫丁香苷在活性氧（ROS）诱导的ALI中的生物学作用。此外，用SIRT1抑制剂EX527或铁死亡激活剂艾拉司丁进一步处理HO刺激的A549细胞，以阐明紫丁香苷是否可通过SIRT1/STAT6信号介导的铁死亡抑制对ROS诱导的ALI发挥保护作用。
证实紫丁香苷处理通过激活SIRT1/STAT6信号通路改善了HO刺激的A549肺上皮细胞受损的活力，减轻了炎症反应和氧化应激。紫丁香苷处理通过激活SIRT1/STAT6信号通路抑制了HO刺激的A549肺上皮细胞的铁死亡。用SIRT1抑制剂EX527或铁死亡激活剂艾拉司丁处理均逆转了紫丁香苷对HO诱导的A549肺上皮细胞损伤的缓解作用。
综上所述，紫丁香苷处理通过激活SIRT1/STAT6信号通路抑制铁死亡来减轻HO诱导的肺上皮细胞损伤。
