Next Article in Journal
A Topology-Centric View on Mitotic Chromosome Architecture
Next Article in Special Issue
The Screening of Anticholinergic Accumulation by Traditional Chinese Medicine
Previous Article in Journal
Galectins and Carcinogenesis: Their Role in Head and Neck Carcinomas and Thyroid Carcinomas
Article Menu
Issue 12 (December) cover image

Export Article

Open AccessArticle
Int. J. Mol. Sci. 2017, 18(12), 2744;

Tussilagone Inhibits the Inflammatory Response and Improves Survival in CLP-Induced Septic Mice

Nano-Bio Resources Center, Department of Cosmetic Sciences, Sookmyung Women’s University, Seoul 04310, Korea
Department of Integrative Medical Sciences, Nambu University, Gwangju 506-706, Korea
Department of Convergence Medicine, Asan Institute for Life Sciences, University of Ulsan College of Medicine, Asan Medical Center, 88 Olympic-ro 43-gil, Songpa-gu, Seoul 05505, Korea
College of Pharmacy and Natural Medicine Research Institute, Mokpo National University, Muan, Jeonnam 58554, Korea
These authors contributed equally to this work.
Authors to whom correspondence should be addressed.
Received: 21 November 2017 / Revised: 10 December 2017 / Accepted: 13 December 2017 / Published: 18 December 2017
(This article belongs to the Special Issue Traditional Medicine – Unraveling Its Molecular Mechanism)
Full-Text   |   PDF [3416 KB, uploaded 18 December 2017]   |  


Tussilagone, extracted from Tussilago farfara is an oriental medicine used for asthma and bronchitis. We investigated its mechanism of action, its inhibitory effects on lipopolysaccharide-induced inflammation in macrophages, and its impact on viability in a cecal ligation and puncture (CLP)-induced mouse model of sepsis. Tussilagone suppressed the expression of the inflammatory mediators, nitric oxide and prostaglandin E2, and the inflammatory cytokines, tumor necrosis factor-alpha (TNF-α) and high-mobility group box 1 (HMGB1), in lipopolysaccharide-stimulated RAW 264.7 cells and peritoneal macrophages. Tussilagone also reduced the activation of the mitogen-activated protein kinases and nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) involved in the activation of various inflammatory mediators in activated macrophages. Moreover, tussilagone administration (1 mg/kg and 10 mg/kg) produced decreased mortality and lung injury in CLP-activated septic mice. Augmented expression of cyclooxygenase (COX)-2 and TNF-α in pulmonary alveolar macrophages of septic mice were attenuated by tussilagone administration. Tussilagone also suppressed the induction of nitric oxide, prostaglandin E2, TNF-α and HMGB1 in the serum of the septic mice. Overall, tussilagone exhibited protective effects against inflammation and polymicrobial sepsis by suppressing inflammatory mediators possibly via the inhibition of NF-κB activation and the MAP kinase pathway. These results suggest the possible use of tussilagone for developing novel therapeutic modalities for sepsis and other inflammatory diseases. View Full-Text
Keywords: tussilagone; NF-κB; sepsis; inflammation; macrophage tussilagone; NF-κB; sepsis; inflammation; macrophage

Graphical abstract

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 (CC BY 4.0).

Share & Cite This Article

MDPI and ACS Style

Kim, Y.K.; Yeo, M.G.; Oh, B.K.; Kim, H.Y.; Yang, H.J.; Cho, S.-S.; Gil, M.; Lee, K.J. Tussilagone Inhibits the Inflammatory Response and Improves Survival in CLP-Induced Septic Mice. Int. J. Mol. Sci. 2017, 18, 2744.

Show more citation formats Show less citations formats

Note that from the first issue of 2016, MDPI journals use article numbers instead of page numbers. See further details here.

Related Articles

Article Metrics

Article Access Statistics



[Return to top]
Int. J. Mol. Sci. EISSN 1422-0067 Published by MDPI AG, Basel, Switzerland RSS E-Mail Table of Contents Alert
Back to Top