Regulatory Effect of Cinnamaldehyde on Monocyte/Macrophage-Mediated Inflammatory Responses

Cinnamaldehyde (CA) has been known to exhibit anti-inflammatory and anticancer effects. Although numerous pharmacological effects have been demonstrated, regulatory effect of CA on the functional activation of monocytes and macrophages has not been fully elucidated yet. To evaluate its monocyte/mac...

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Main Authors: Byung Hun Kim, Yong Gyu Lee, Jaehwi Lee, Joo Young Lee, Jae Youl Cho
Format: Article
Language:English
Published: Wiley 2010-01-01
Series:Mediators of Inflammation
Online Access:http://dx.doi.org/10.1155/2010/529359
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author Byung Hun Kim
Yong Gyu Lee
Jaehwi Lee
Joo Young Lee
Jae Youl Cho
author_facet Byung Hun Kim
Yong Gyu Lee
Jaehwi Lee
Joo Young Lee
Jae Youl Cho
author_sort Byung Hun Kim
collection DOAJ
description Cinnamaldehyde (CA) has been known to exhibit anti-inflammatory and anticancer effects. Although numerous pharmacological effects have been demonstrated, regulatory effect of CA on the functional activation of monocytes and macrophages has not been fully elucidated yet. To evaluate its monocyte/macrophage-mediated immune responses, macrophages activated by lipopolysaccharide (LPS), and monocytes treated with proaggregative antibodies, and extracellular matrix protein fibronectin were employed. CA was able to suppress both the production of nitric oxide (NO) and upregulation of surface levels of costimulatory molecules (CD80 and CD69) and pattern recognition receptors (toll-like receptor 2 (TLR2) and complement receptor (CR3)). In addition, CA also blocked cell-cell adhesion induced by the activation of CD29 and CD43 but not cell-fibronectin adhesion. Immunoblotting analysis suggested that CA inhibition was due to the inhibition of phosphoinositide-3-kinase (PI3K) and phosphoinositide-dependent kinase (PDK)1 as well as nuclear factor-(NF-) κB activation. In particular, thiol compounds with sulphydryl group, L-cysteine and dithiothreitol (DTT), strongly abrogated CA-mediated NO production and NF-κB activation. Therefore, our results suggest that CA can act as a strong regulator of monocyte/macrophage-mediated immune responses by thiolation of target cysteine residues in PI3K or PDK1.
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spelling doaj-art-cf98d88438ec45fa9646a48c28d16c5f2025-08-20T03:19:45ZengWileyMediators of Inflammation0962-93511466-18612010-01-01201010.1155/2010/529359529359Regulatory Effect of Cinnamaldehyde on Monocyte/Macrophage-Mediated Inflammatory ResponsesByung Hun Kim0Yong Gyu Lee1Jaehwi Lee2Joo Young Lee3Jae Youl Cho4School of Bioscience and Biotechnology, Institute of Bioscience and Biotechnology, Kangwon National University, Chuncheon 200-701, South KoreaSchool of Bioscience and Biotechnology, Institute of Bioscience and Biotechnology, Kangwon National University, Chuncheon 200-701, South KoreaCollege of Pharmacy, Chung-Ang University, Seoul 156-756, South KoreaDepartment of Life Sciences and Research Center for Biomedical Nanotechnology, Gwangju Institute of Science and Technology, Gwangju 500-712, South KoreaSchool of Bioscience and Biotechnology, Institute of Bioscience and Biotechnology, Kangwon National University, Chuncheon 200-701, South KoreaCinnamaldehyde (CA) has been known to exhibit anti-inflammatory and anticancer effects. Although numerous pharmacological effects have been demonstrated, regulatory effect of CA on the functional activation of monocytes and macrophages has not been fully elucidated yet. To evaluate its monocyte/macrophage-mediated immune responses, macrophages activated by lipopolysaccharide (LPS), and monocytes treated with proaggregative antibodies, and extracellular matrix protein fibronectin were employed. CA was able to suppress both the production of nitric oxide (NO) and upregulation of surface levels of costimulatory molecules (CD80 and CD69) and pattern recognition receptors (toll-like receptor 2 (TLR2) and complement receptor (CR3)). In addition, CA also blocked cell-cell adhesion induced by the activation of CD29 and CD43 but not cell-fibronectin adhesion. Immunoblotting analysis suggested that CA inhibition was due to the inhibition of phosphoinositide-3-kinase (PI3K) and phosphoinositide-dependent kinase (PDK)1 as well as nuclear factor-(NF-) κB activation. In particular, thiol compounds with sulphydryl group, L-cysteine and dithiothreitol (DTT), strongly abrogated CA-mediated NO production and NF-κB activation. Therefore, our results suggest that CA can act as a strong regulator of monocyte/macrophage-mediated immune responses by thiolation of target cysteine residues in PI3K or PDK1.http://dx.doi.org/10.1155/2010/529359
spellingShingle Byung Hun Kim
Yong Gyu Lee
Jaehwi Lee
Joo Young Lee
Jae Youl Cho
Regulatory Effect of Cinnamaldehyde on Monocyte/Macrophage-Mediated Inflammatory Responses
Mediators of Inflammation
title Regulatory Effect of Cinnamaldehyde on Monocyte/Macrophage-Mediated Inflammatory Responses
title_full Regulatory Effect of Cinnamaldehyde on Monocyte/Macrophage-Mediated Inflammatory Responses
title_fullStr Regulatory Effect of Cinnamaldehyde on Monocyte/Macrophage-Mediated Inflammatory Responses
title_full_unstemmed Regulatory Effect of Cinnamaldehyde on Monocyte/Macrophage-Mediated Inflammatory Responses
title_short Regulatory Effect of Cinnamaldehyde on Monocyte/Macrophage-Mediated Inflammatory Responses
title_sort regulatory effect of cinnamaldehyde on monocyte macrophage mediated inflammatory responses
url http://dx.doi.org/10.1155/2010/529359
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