Planta Med 2019; 85(04): 302-311
DOI: 10.1055/a-0777-2420
Biological and Pharmacological Activity
Original Papers
Georg Thieme Verlag KG Stuttgart · New York

Anti-Inflammatory Activity of Lobaric Acid via Suppressing NF-κB/MAPK Pathways or NLRP3 Inflammasome Activation

Hee-Weon Lee
1   School of Pharmacy, Sungkyunkwan University, Suwon, Republic of Korea
,
JinWook Kim
1   School of Pharmacy, Sungkyunkwan University, Suwon, Republic of Korea
,
Joung-Han Yim
2   Polar BioCenter, Korea Polar Research Institute, KORDI, Incheon, Republic of Korea
,
Hong-Kum Lee
2   Polar BioCenter, Korea Polar Research Institute, KORDI, Incheon, Republic of Korea
,
Suhkneung Pyo
1   School of Pharmacy, Sungkyunkwan University, Suwon, Republic of Korea
› Institutsangaben
Weitere Informationen

Publikationsverlauf

received 26. Mai 2018
revised 19. Oktober 2018

accepted 25. Oktober 2018

Publikationsdatum:
16. November 2018 (online)


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Abstract

Lobaric acid (LA) is a constituent of the lichen Stereocaulon alpinum. LA has multiple biological activities, including antibacterial and antioxidant ones. The purpose of this study was to investigate the effect of LA and its mechanism on lipopolysaccharide (LPS)-induced inflammatory responses in macrophages. Macrophages were pretreated with different concentrations of LA (0.2 – 20 µM), followed by LPS stimulation. LA treatment of LPS stimulated macrophages decreased their nitric oxide production and the expression of cyclooxygenase-2 and prostaglandin E2. LA also significantly reduced the production of tumor necrosis factor-α and interleukin (IL)-6 by inhibiting the activation of mitogen-activated protein kinases (MAPKs) and nuclear factor-kappa B (NF-κB). Additionally, LA inhibited the production of IL-1β and IL-18, as well as caspase-1 maturation, by inhibition of NLRP3 inflammasome activation in LPS/ATP-stimulated cells. These results strongly suggest that LA could inhibit inflammation by downregulating NF-κB/MAPK pathways and NLRP3 inflammasome activation in activated macrophages. These results reveal a new therapeutic approach to modulate inflammatory diseases linked to deregulated inflammasome activities.

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