Paeonol Attenuates Cigarette Smoke-Induced Lung Inflammation by Inhibiting ROS-Sensitive Inflammatory SignalingReport as inadecuate

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Mediators of InflammationVolume 2014 2014, Article ID 651890, 13 pages

Research Article

Department of Physiology, School of Medicine, National Yang-Ming University, Taipei 11221, Taiwan

Department of Neurosurgery, Cheng Hsin General Hospital, Taipei 11220, Taiwan

Department of Chest Medicine, Taipei Veterans General Hospital, Taipei 11217, Taiwan

Received 27 May 2014; Revised 14 July 2014; Accepted 15 July 2014; Published 3 August 2014

Academic Editor: Yuh-Lien Chen

Copyright © 2014 Meng-Han Liu et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Cigarette smoking causes persistent lung inflammation that is mainly regulated by redox-sensitive pathways. We have previously reported that cigarette smoke CS activates reactive oxygen species- ROS- sensitive mitogen-activated protein kinases MAPKs-nuclear factor-κB NF-κB signaling leading to induction of lung inflammation. Paeonol, the main phenolic compound present in the Chinese herb Paeonia suffruticosa, has antioxidant and anti-inflammatory properties. However, whether paeonol has similar beneficial effects against CS-induced lung inflammation remains unclear. Using a murine model, we showed that chronic CS exposure for 4 weeks caused pulmonary inflammatory infiltration, increased lung vascular permeability, elevated lung levels of chemokines, cytokines, and 4-hydroxynonenal an oxidative stress biomarker, and induced lung inflammation; all of these CS-induced events were suppressed by chronic treatment with paeonol. Using human bronchial epithelial cells HBECs, we demonstrated that cigarette smoke extract CSE sequentially increased extracellular and intracellular levels of ROS, activated the MAPKs-NF-κB signaling, and induced interleukin-8 IL-8; all these CSE-induced events were inhibited by paeonol pretreatment. Our findings suggest a novel role for paeonol in alleviating the oxidative stress and lung inflammation induced by chronic CS exposure in vivo and in suppressing CSE-induced IL-8 in vitro via its antioxidant function and an inhibition of the MAPKs-NF-κB signaling.

Author: Meng-Han Liu, An-Hsuan Lin, Hung-Fu Lee, Hsin-Kuo Ko, Tzong-Shyuan Lee, and Yu Ru Kou



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