Table I.
Potential mechanism underlying the effects or progression pathways of CAPE in its anti-inflammatory/immunomodulatory action.
| Mechanism for the effect or progression pathway(s) | In vivo/in vitro | Cells/animals used | Reported outcomes (ref.) |
|---|---|---|---|
| Inhibiting ROS production; suppressing NF-κB activation | In vivo, EAE (animal model of MS) | Rats | Inhibited ROS production (XO activity, levels of MDA); reduced infiltration of inflammatory cells (22) |
| Suppressing inflammation and ocular tissue damage | In vivo, LPS-induced inflammation | Rats | Suppressed number of inflammatory cells and MPO activity (46) |
| Inhibiting NF-κB activation and mRNA expression; preventing degradation and phosphorylation of p65; suppressed of p65 subunit | In vitro, cell culture; in vivo, H. pylori-induced chronic gastritis | AGS cells, Mongolian gerbils | Inhibited NF-κB activation by suppression of IκB-α degradation of IκB-α and phosphorylation NF-κB p50; reduced mRNA expression of TNF-α, IL-2, IL-6, iNOS and KC (23) |
| Inhibiting NF-κB transcriptional activation | In vitro | Jurkat, MT2 human T-cell lines | Inhibited NF-κB transcriptional activation induced by Tax (47) |
| Inhibiting TNF-α-dependent NF-κB activation via direct inhibition of IKK as well as activation of the Nrf2 pathway | In vitro, cell culture | HCT116 (human coloncarcinoma) cells | Inhibited NF-κB activation by TNF-α and LPS, and directly inhibited IKK in HCT116 cells. Nrf2 activation is associated with the inhibition of the NF-κB pathway (48) |
| Inhibiting the inflammatory pathway | In vivo | Mice | Reduced NF-κB activation and levels of COX-2 (49) |
| Inhibiting cytokine and chemokine production associated with the NF-κB signaling pathway | In vitro, peripheral blood sampling | MoDCs | Inhibited cytokine and chemokine production, IκB-α phosphorylation and NF-κB activation in human MoDCs (50) |
| Inhibiting gene expression of proinflammatory cytokines from LPS-stimulated macrophages | In vitro, cell culture | LPS-stimulated RAW264.7 cells | Reduced mRNA expression of MCP-1, TNF-α, IL-6 and IL-1β (35) |
| Blocking NF-κB-dependent activation of the inflammatory responses | In vivo, eccentric exercise-induced skeletal muscle injury | Rats | Suppressed high COX-2 and iNOS expression and IL-1β and MCP-1 levels (34) |
| Anti-inflammatory action on rat burn healing | In vivo, burn injury | Rats | Reduced MPO activity, NO levels and CD68 expression; improved wound healing after burn (30) |
CAPE, caffeic acid phenethyl ester; CD68, cluster of differentiation 68; COX-2, cyclooxygenase-2; EAE, experimental autoimmune encephalomyelitis; IκB-α, κB inhibitor-α; IKK, IκB-kinase; IL, interleukin; iNOS, inducible nitric oxide synthase; LPS, lipopolysaccharide; MCP-1, monocyte chemoattractant protein-1; MDA, malondialdehyde; MODC, monocyte-derived dendritic cell; MPO, myeloperoxidase; MS, multiple sclerosis; NF-κB, nuclear factor κB; Nrf2, nuclear-factor-E2-related factor 2; ROS, reactive oxygen species; TNF-α, tumor necrosis factor-α; XO, xanthine oxidase.