Planta Med 2015; 81(01): 39-45
DOI: 10.1055/s-0034-1383361
Biological and Pharmacological Activity
Original Papers
Georg Thieme Verlag KG Stuttgart · New York

Bornyl Cinnamate Inhibits Inflammation-Associated Gene Expression in Macrophage Cells through Suppression of Nuclear Factor-κB Signaling Pathway

Kanthasamy Jayabal Senthil Kumar
1   Department of Forestry, National Chung Hsing University, Taichung, Taiwan
,
Justine Li
2   Department of Neurobiology and Behavior, Department of Psychology, College of Arts and Sciences, Honors College, Stony Brook University, New York, USA
,
Muthuraj Gokila Vani
1   Department of Forestry, National Chung Hsing University, Taichung, Taiwan
,
Yu-Hsin Hsieh
3   Department of Food Science and Technology, College of Agriculture and Environmental Sciences, University of California, Davis, CA, USA
,
Yueh-Hsiung Kuo
4   Graduate Institute of Chinese Pharmaceutical Science, China Medical University, Taichung, Taiwan
5   Department of Biotechnology, Asia University, Taichung, Taiwan
,
Sheng-Yang Wang
1   Department of Forestry, National Chung Hsing University, Taichung, Taiwan
6   Agricultural Biotechnology Center, National Chung-Hsing University, Taichung, Taiwan
7   Agricultural Biotechnology Research Institute, Academia Sinica, Taipei, Taiwan
› Author Affiliations
Further Information

Publication History

received 29 September 2014
revised 04 November 2014

accepted 10 November 2014

Publication Date:
17 December 2014 (online)

Abstract

Formosan sweetgum (Liquidamber formosana) is an endemic tree species. Various parts of this tree are used as a traditional Chinese medicine for treating pain, inflammation, and rheumatic disorders. In this study, we investigated the anti-inflammatory potential of bornyl cinnamate, a cinnamic acid derivative from the essential oil of L. formosana. Pretreatment with bornyl cinnamate significantly inhibited lipopolysaccharide-induced proinflammatory molecules, including nitric oxide, prostaglandin-E2, tumor necrosis factor α, and interleukin-1β production, in murine macrophage RAW 264.7 cells. RT-PCR and immunoblotting analysis revealed that the inhibition of the proinflammatory molecules occurred through the downregulation of their corresponding mediator genes. Immunofluorescence and luciferase reporter assays revealed that the inhibition of proinflammatory genes by bornyl cinnamate was caused by the suppression of nuclear translocation and transcriptional activation of the redox-sensitive transcription factor nuclear factor κB. In addition, bornyl cinnamate increased the protein stability of the inhibitor of nuclear factor κB, an endogenous repressor of nuclear factor κB, through inhibition of its phosphorylation and proteasomal degradation. Furthermore, bornyl cinnamate significantly blocked the lipopolysaccharide-induced activation of I-κB kinase α, an upstream kinase of the inhibitor of nuclear factor κB α. Taken together, these results suggest that bornyl cinnamate could inhibit proinflammatory molecules through the suppression of the redox-sensitive nuclear factor κB signaling pathway.

 
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