| Literature DB >> 26466890 |
Po-Len Liu1, Inn-Wen Chong1,2, Yi-Chen Lee1, Jong-Rung Tsai1,2, Hui-Min Wang1, Chong-Chao Hsieh2, Hsuan-Fu Kuo3, Wei-Lun Liu4, Yung-Hsiang Chen5,6,7, Hsiu-Lin Chen1,2.
Abstract
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.Entities:
Keywords: hypoxia; inflammation; reoxygenation; resveratrol; surfactant
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Year: 2015 PMID: 26466890 DOI: 10.1021/acs.jafc.5b01168
Source DB: PubMed Journal: J Agric Food Chem ISSN: 0021-8561 Impact factor: 5.279