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Int. J. Mol. Sci. 2017, 18(12), 2744; doi:10.3390/ijms18122744

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

1
Nano-Bio Resources Center, Department of Cosmetic Sciences, Sookmyung Women’s University, Seoul 04310, Korea
2
Department of Integrative Medical Sciences, Nambu University, Gwangju 506-706, Korea
3
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
4
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)
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Abstract

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
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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.

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