Department of Respiratory Therapy, Department of Fragrance and Cosmetic Science, College of Medicine, Kaohsiung Medical University , Kaohsiung 807, Taiwan.
Department of Pediatrics, Department of Internal Medicine, Department of Chest Surgery, Division of Cardiovascular Surgery, Department of Surgery, Kaohsiung Medical University Hospital , Kaohsiung 807, Taiwan.
J Agric Food Chem. 2015 Nov 4;63(43):9480-7. doi: 10.1021/acs.jafc.5b01168. Epub 2015 Oct 22.
Reducing oxidative stress is crucial to prevent hypoxia-reoxygenation (H/R)-induced lung injury. Resveratrol has excellent antioxidant and anti-inflammatory effects, and this study investigated its role in H/R-induced type II pneumocyte dysfunction. H/R conditions increased expression of inflammatory cytokines including interleukin (IL)-1β (142.3 ± 21.2%, P < 0.05) and IL-6 (301.9 ± 35.1%, P < 0.01) in a type II alveolar epithelial cell line (A549), while the anti-inflammatory cytokine IL-10 (64.6 ± 9.8%, P < 0.05) and surfactant proteins (SPs) decreased. However, resveratrol treatment effectively inhibited these effects. H/R significantly activated an inflammatory transcription factor, nuclear factor (NF)-κB, while resveratrol significantly inhibited H/R-induced NF-κB transcription activities. To the best of our knowledge, this is the first study showing resveratrol-mediated reversal of H/R-induced inflammatory responses and dysfunction of type II pneumocyte cells in vitro. The effects of resveratrol were partially mediated by promoting SP expression and inhibiting inflammation with NF-κB pathway involvement. Therefore, our study provides new insights into mechanisms underlying the action of resveratrol in type II pneumocyte dysfunction.
减轻氧化应激对于预防缺氧复氧（H/R）诱导的肺损伤至关重要。白藜芦醇具有出色的抗氧化和抗炎作用，本研究探讨了其在 H/R 诱导的 II 型肺泡上皮细胞功能障碍中的作用。H/R 条件增加了炎症细胞因子的表达，包括白细胞介素（IL）-1β（142.3 ± 21.2%，P < 0.05）和 IL-6（301.9 ± 35.1%，P < 0.01），在 II 型肺泡上皮细胞系（A549）中，而抗炎细胞因子 IL-10（64.6 ± 9.8%，P < 0.05）和表面活性剂蛋白（SP）减少。然而，白藜芦醇处理可有效抑制这些作用。H/R 显著激活了炎症转录因子核因子（NF）-κB，而白藜芦醇显著抑制了 H/R 诱导的 NF-κB 转录活性。据我们所知，这是第一项显示白藜芦醇介导的体外 H/R 诱导的炎症反应和 II 型肺泡上皮细胞功能障碍逆转的研究。白藜芦醇的作用部分是通过促进 SP 表达和抑制炎症以及 NF-κB 途径参与来实现的。因此，我们的研究为白藜芦醇在 II 型肺泡上皮细胞功能障碍中的作用机制提供了新的见解。
