Antiinflammatory Activity of Cinnamon (Cinnamomum zeylanicum) Bark Essential Oil in a Human Skin Disease Model

Abstract

The effect of cinnamon (Cinnamomum zeylanicum) bark essential oil (CBEO) on human skin cells has not been elucidated. Therefore, we investigated the activity of a commercially available CBEO in a validated human dermal fibroblast system, a model of chronic inflammation and fibrosis. We first evaluated the impact of CBEO on 17 protein biomarkers that play critical roles in inflammation and tissue remodeling. The impact of CBEO on genome-wide gene expression was also evaluated. CBEO showed strong anti-proliferative effects on skin cells and significantly inhibited the production of several inflammatory biomarkers, including vascular cell adhesion molecule-1, intercellular cell adhesion molecule-1, monocyte chemoattractant protein-1, interferon gamma-induced protein 10, interferon-inducible T-cell alpha chemoattractant, and monokine induced by gamma interferon. In addition, CBEO significantly inhibited the production of several tissue remodeling molecules, including epidermal growth factor receptor, matrix metalloproteinase-1, and plasminogen activator inhibitor-1. Macrophage colony-stimulating factor, which is an immunomodulatory protein molecule, was also significantly inhibited by CBEO. Furthermore, CBEO significantly modulated global gene expression and altered signaling pathways, many of which are important in inflammation, tissue remodeling, and cancer biology. The study shows that CBEO is a promising antiinflammatory agent; however, further research is required to clarify its clinical efficacy. © 2017 The Authors. Phytotherapy Research published by John Wiley & Sons Ltd.

Keywords: MIG; VCAM-1; cell proliferation; cinnamon bark essential oil; genome-wide gene expression; inflammation.

Figure 1

The bioactivity profile of cinnamon bark essential oil (0.0012% v/v) in the human dermal fibroblast system HDF3CGF. The x‐axis denotes protein‐based biomarker readouts. The y‐axis denotes the relative expression levels of biomarkers when compared with the values for the vehicle control in log form. Vehicle control values are marked in gray at a 95% confidence level. * indicates a biomarker designated as having ‘key activity’, which is when a biomarker value is significantly different (p < 0.01) from the respective value for the vehicle control at a studied concentration, with an effect size of at least 20% (more than 0.1 log ratio units). MCP‐1, monocyte chemoattractant protein; VCAM‐1, vascular cell adhesion molecule 1; ICAM‐1, intracellular cell adhesion molecule 1; IP‐10, interferon gamma‐induced protein 10; I‐TAC, interferon‐inducible T‐cell alpha chemoattractant; IL‐8, interleukin‐8; MIG, the monokine induced by gamma interferon; EGFR, epidermal growth factor receptor; M‐CSF, macrophage colony‐stimulating factor; MMP‐1, matrix metalloproteinase 1; PAI‐1, plasminogen activator inhibitor 1; TIMP, tissue inhibitor of metalloproteinase.

Figure 2

Top 20 canonical pathways matching the bioactivity profile of cinnamon bark essential oil (0.0012% v/v) in gene expression in the HDF3CGF system, as obtained from the IPA. The p‐values were calculated using right‐tailed Fisher's exact test. Each p‐value measures how likely an observed association between a specific pathway and the dataset would be if it were only due to a random chance. The smaller the p‐value [bigger – ln (p‐value), indicated by the black bars] for a pathway is, the more significantly it matches with the bioactivity of CBEO. A ratio, indicated by the gray bar, was calculated by dividing the number of genes from the CBEO dataset that participated in a canonical pathway by the total number of genes in that pathway. NRF2, nuclear factor E2‐related factor 2; CHK, checkpoint kinase; PPAR, peroxisome proliferator‐activated receptor; Cdc 42, cell division control protein 42 homolog; BRCA1, breast cancer type 1 susceptibility protein; ERK5, extracellular signal‐regulated kinase 5.