Curcumin Attenuates Airway Inflammation and Airway Remolding by Inhibiting NF-κB Signaling and COX-2 in Cigarette Smoke-Induced COPD Mice
The purpose of this study is to evaluate the therapeutic effects of curcumin on airway inflammation using LPS and cigarette smoke (LC)-induced COPD murine models and LPS-stimulated human bronchial epithelial (BEAS-2B) cells. In this research, COPD murine models were established after challenged with LPS for 2 days and exposed to cigarette smoke for 35 days. Treatment with curcumin for 10 days distinctly alleviated airway inflammation and airway remolding in LC-induced COPD mice according to the lung H&E histopathological examination. The number of neutrophils and lymphocytes in broncho alveolar lavage fluid (BALF) was significantly decreased in curcumin+LC-treated group compared with the LC-induced mice. Additionally, curcumin inhibited BEAS-2B cells proliferation, which suggested the preventive effect of curcumin on progressive airway remolding and inflammatory response mediated by bronchial epithelial cells. Further investigation demonstrated an underlying molecular mechanism for the therapeutic effects of curcumin may rely on the inhibition of the degradation of IκBα and COX-2 expression in curcumin+LC-treated COPD mice and LPS-stimulated BEAS-2B cells. Overall, curcumin alleviates the airway inflammation and airway remolding, which is closely related to inhibit the BEAS-2B cells proliferation and suppress the activation of NF-κB and COX-2 expression. These findings indicate that curcumin may be a potential agent for the therapy of COPD.
KEY WORDSCurcumin COPD NF-κB COX-2 Inflammation
Chronic obstructive pulmonary disease
Bronchoalveolar lavage fluid
Phosphate-buffered physiological saline
LPS + cigarette smoke
Transforming growth factor-β
Bronchial epithelial cells
This work was supported by the Department of Science and Technology Program Funds of Jiangxi Province, China (No. 20151BAB205085).
Compliance with Ethical Standards
The entire experiments were reviewed and proved by the Institutional Animal Experimental Ethics Committee of Nanchang University.
Conflict of Interest
The authors declare that they have no conflicts of interest.
- 1.Organization, W.H., WHO. 2013. the top 10 causes of death. Countries.Google Scholar
- 10.Cheng, J., R.T. Dackor, J.A. Bradbury, H. Li, L.M. DeGraff, L.K. Hong, D. King, F.B. Lih, A. Gruzdev, M.L. Edin, G.S. Travlos, G.P. Flake, K.B. Tomer, and D.C. Zeldin. 2016. Contribution of alveolar type II cell-derived cyclooxygenase-2 to basal airway function, lung inflammation, and lung fibrosis. The FASEB Journal 30 (1): 160–173.CrossRefPubMedGoogle Scholar
- 13.Brouk, B. 1975. Plants consumed by man. QUARTERLY REVIEW OF BIOLOGY.Google Scholar
- 15.Lee, I.T., and C.-M. Yang. 2013. Inflammatory signalings involved in airway and pulmonary diseases. Mediators of Inflammation 2013: 1–12.Google Scholar
- 18.Wang, J., et al. 2017. Regulation of type II collagen, matrix metalloproteinase-13 and cell proliferation by interleukin-1β is mediated by curcumin via inhibition of NF-κB signaling in rat chondrocytes. Molecular Medicine Reports.Google Scholar
- 21.Liu, R., P. Wang, C. Wu, J. Chen, C. Li, Y. Xie, Q. Wang, J. Liu, H. He, and J. Zhu. 2017. Therapeutic effects of Hedyotis diffusa Willd in a COPD mouse model challenged with LPS and smoke. Experimental and Therapeutic Medicine.Google Scholar
- 24.Anto, R.J., A. Mukhopadhyay, S. Shishodia, C.G. Gairola, and B.B. Aggarwal. 2002. Cigarette smoke condensate activates nuclear transcription factor-κB through phosphorylation and degradation of IκBα: Correlation with induction of cyclooxygenase-2. Carcinogenesis 23 (9): 1511–1518.CrossRefPubMedGoogle Scholar
- 26.Liu, W., H.L. Jiang, L.L. Cai, M. Yan, S.J. Dong, and B. Mao. 2016. Tanreqing injection attenuates lipopolysaccharide-induced airway inflammation through MAPK/NF-kappaB signaling pathways in rats model. Evidence-based Complementary and Alternative Medicine 2016: 5292346.PubMedPubMedCentralGoogle Scholar
- 27.Hardaker, E.L., M.S. Freeman, N. Dale, P. Bahra, F. Raza, K.H. Banner, and C. Poll. 2010. Exposing rodents to a combination of tobacco smoke and lipopolysaccharide results in an exaggerated inflammatory response in the lung. British Journal of Pharmacology 160 (8): 1985–1996.CrossRefPubMedPubMedCentralGoogle Scholar
- 28.Shu, J., D. Li, H. Ouyang, J. Huang, Z. Long, Z. Liang, Y. Chen, Y. Chen, Q. Zheng, M. Kuang, H. Tang, J. Wang, and W. Lu. 2017. Comparison and evaluation of two different methods to establish the cigarette smoke exposure mouse model of COPD. Scientific Reports 7 (1): 15454.CrossRefPubMedPubMedCentralGoogle Scholar
- 35.Hernandez, M.L., B. Harris, J.C. Lay, P.A. Bromberg, D. Diaz-Sanchez, R.B. Devlin, S.R. Kleeberger, N.E. Alexis, and D.B. Peden. 2010. Comparative airway inflammatory response of normal volunteers to ozone and lipopolysaccharide challenge. Inhalation Toxicology 22 (8): 648–656.CrossRefPubMedPubMedCentralGoogle Scholar
- 40.Cohen, L., X. E, J. Tarsi, T. Ramkumar, T.K. Horiuchi, R. Cochran, S. DeMartino, K.B. Schechtman, I. Hussain, M.J. Holtzman, M. Castro, and and the NHLBI Severe Asthma Research Program (SARP). 2007. Epithelial cell proliferation contributes to airway remodeling in severe asthma. American Journal of Respiratory and Critical Care Medicine 176 (2): 138–145.CrossRefPubMedPubMedCentralGoogle Scholar