Paeonol Attenuates Cigarette Smoke-Induced Lung Inflammation by Inhibiting ROS-Sensitive Inflammatory Signaling
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...
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| Main Authors: | , , , , , |
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| Format: | Article |
| Language: | English |
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Wiley
2014-01-01
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| Series: | Mediators of Inflammation |
| Online Access: | http://dx.doi.org/10.1155/2014/651890 |
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| author | Meng-Han Liu An-Hsuan Lin Hung-Fu Lee Hsin-Kuo Ko Tzong-Shyuan Lee Yu Ru Kou |
| author_facet | Meng-Han Liu An-Hsuan Lin Hung-Fu Lee Hsin-Kuo Ko Tzong-Shyuan Lee Yu Ru Kou |
| author_sort | Meng-Han Liu |
| collection | DOAJ |
| description | 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. |
| format | Article |
| id | doaj-art-c6f0d83e4ae041ac9f7bdef107fd89eb |
| institution | DOAJ |
| issn | 0962-9351 1466-1861 |
| language | English |
| publishDate | 2014-01-01 |
| publisher | Wiley |
| record_format | Article |
| series | Mediators of Inflammation |
| spelling | doaj-art-c6f0d83e4ae041ac9f7bdef107fd89eb2025-08-20T03:22:58ZengWileyMediators of Inflammation0962-93511466-18612014-01-01201410.1155/2014/651890651890Paeonol Attenuates Cigarette Smoke-Induced Lung Inflammation by Inhibiting ROS-Sensitive Inflammatory SignalingMeng-Han Liu0An-Hsuan Lin1Hung-Fu Lee2Hsin-Kuo Ko3Tzong-Shyuan Lee4Yu Ru Kou5Department of Physiology, School of Medicine, National Yang-Ming University, Taipei 11221, TaiwanDepartment of Physiology, School of Medicine, National Yang-Ming University, Taipei 11221, TaiwanDepartment of Neurosurgery, Cheng Hsin General Hospital, Taipei 11220, TaiwanDepartment of Physiology, School of Medicine, National Yang-Ming University, Taipei 11221, TaiwanDepartment of Physiology, School of Medicine, National Yang-Ming University, Taipei 11221, TaiwanDepartment of Physiology, School of Medicine, National Yang-Ming University, Taipei 11221, TaiwanCigarette 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.http://dx.doi.org/10.1155/2014/651890 |
| spellingShingle | Meng-Han Liu An-Hsuan Lin Hung-Fu Lee Hsin-Kuo Ko Tzong-Shyuan Lee Yu Ru Kou Paeonol Attenuates Cigarette Smoke-Induced Lung Inflammation by Inhibiting ROS-Sensitive Inflammatory Signaling Mediators of Inflammation |
| title | Paeonol Attenuates Cigarette Smoke-Induced Lung Inflammation by Inhibiting ROS-Sensitive Inflammatory Signaling |
| title_full | Paeonol Attenuates Cigarette Smoke-Induced Lung Inflammation by Inhibiting ROS-Sensitive Inflammatory Signaling |
| title_fullStr | Paeonol Attenuates Cigarette Smoke-Induced Lung Inflammation by Inhibiting ROS-Sensitive Inflammatory Signaling |
| title_full_unstemmed | Paeonol Attenuates Cigarette Smoke-Induced Lung Inflammation by Inhibiting ROS-Sensitive Inflammatory Signaling |
| title_short | Paeonol Attenuates Cigarette Smoke-Induced Lung Inflammation by Inhibiting ROS-Sensitive Inflammatory Signaling |
| title_sort | paeonol attenuates cigarette smoke induced lung inflammation by inhibiting ros sensitive inflammatory signaling |
| url | http://dx.doi.org/10.1155/2014/651890 |
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