2. Academic Validation
  3. Tussilagone Inhibits the Inflammatory Response and Improves Survival in CLP-Induced Septic Mice

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

  • Int J Mol Sci. 2017 Dec 18;18(12):2744. doi: 10.3390/ijms18122744.
Yun Kyu Kim 1,  Myeong Gu Yeo 2,  Bo Kang Oh 3,  Ha Yeong Kim 4,  Hun Ji Yang 5,  Seung-Sik Cho 6,  Minchan Gil 7,  Kyung Jin Lee 8
Affiliations

Affiliations

  • 1 Nano-Bio Resources Center, Department of Cosmetic Sciences, Sookmyung Women's University, Seoul 04310, Korea. kingsagayo@gmail.com.
  • 2 Department of Integrative Medical Sciences, Nambu University, Gwangju 506-706, Korea. mgy11@nambu.ac.kr.
  • 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. bokang7804@gmail.com.
  • 4 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. kimhayeong0516@gmail.com.
  • 5 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. didgnswl95@gmail.com.
  • 6 College of Pharmacy and Natural Medicine Research Institute, Mokpo National University, Muan, Jeonnam 58554, Korea. sscho@mokpo.ac.kr.
  • 7 Nano-Bio Resources Center, Department of Cosmetic Sciences, Sookmyung Women's University, Seoul 04310, Korea. minchangil@sookmyung.ac.kr.
  • 8 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. kjlee@amc.seoul.kr.
PMID: 29258263 DOI: 10.3390/ijms18122744
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.

Keywords

NF-κB; inflammation; macrophage; sepsis; tussilagone.

Figures
Products