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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| Format: | Article |
| Language: | English |
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Wiley
2010-01-01
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| Series: | Mediators of Inflammation |
| Online Access: | http://dx.doi.org/10.1155/2010/529359 |
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| _version_ | 1849695577891143680 |
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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. |
| format | Article |
| id | doaj-art-cf98d88438ec45fa9646a48c28d16c5f |
| institution | DOAJ |
| issn | 0962-9351 1466-1861 |
| language | English |
| publishDate | 2010-01-01 |
| publisher | Wiley |
| record_format | Article |
| series | Mediators of Inflammation |
| 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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