Table 3.
In vitro anti-inflammatory effects of 6-shogaol.
Cell Type | Concentration | Effects |
---|---|---|
Human HaCaT cells | 0.1, 1, and 10 µM | Reduced release of IL-1β, TNF, IL-6, IL-8 |
Human polymorphonuclear neutrophils | Increasing concentrations | DPPH scavenging: IC50: 8 µM |
6 µM | Reduction of fMLP-induced oxidative burst | |
Murine RAW 264.7 macrophages | 1, 3, 6 µM | Reduction of LPS-induced nitrite and PGE2 release |
Murine RAW 264.7 macrophages | 5 µM | Reduction of LPS-triggered exposition of arachidonic acid and of LPS/IFN-γ-induced NO synthesis |
Murine RAW 264.7 macrophages | 2, 10, and 20 µM | Reduction of LPS-induced TNF, IL-1β, and NO |
Murine RAW 264.7 macrophages | 10–20 µM | Reduction of LPS-triggered mRNA, protein and activation of iNOS and COX-2; reduction of nitrite and PGE2 |
6 and 10 µM | Reduction of NFκB nuclear translocation and IκBα degradation and phosphorylation; inhibition of ERK phosphorylation and PI3K/Akt activation |
|
Human 293T cells | 20 and 30 µM | Reduction of MyD88- and IKKβ-induced NFκB activity |
Murine hematopoietic cell line Ba/F3 | 20 and 30 µM | Block of LPS-activated degradation of IRAK-1 |
30 µM | Block of LPS-induced TLR4 dimerization | |
Primary rat cortical neuron-glia cells | 10 µM | Reduction of LPS-induced NO, iNOS, COX-2 protein, PGE2, IL-1β, and TNF; inhibition of LPS-triggered p38, JNK and ERK phosphorylation and NFκB activity, IκBα phosphorylation and degradation |
Murine microglia cell line BV-2 | 10 µM | Reduction of LPS-induced iNOS, COX-2 |
Human mast cells (HMC-1) | 0.1 and 1 µM | Reduction of TPA/A23187-induced IL-6, IL-8, and TNF release |
50 and 100 µM | Reduction of nuclear NFκB and cytosolic IκBα phosphorylation | |
10 µM | Inhibition of JNK activation | |
Rat peritoneal mast cells | 0.1 µM | Reduction of compound 48/80-induced histamine release |
Murine microglia cell line BV-2 | 5, 10, and 20 µM | Reduction of LPS-activated TNF, IL-1β, PGE2, and IL-6 release, NFκB phosphorylation and translocation into the nucleus, IκBα degradation and phosphorylation; Increase of PPARγ |
Human proximal tubular cell line HK-2 | 50, 100, and 150 µM | Reduction of TNF-induced TNF, IL-6, IL-8, MCP-1, MIP-2, and ICAM-1 mRNA; reduction of H2O2-induced IL-8, MIP-2, TNF, ICAM-1 |
150 µM | Inhibition of TNF-activated nuclear NFκB, pIKK, pIκBα, and IκBα degradation | |
Primary mouse proximal tubule | 50, 100, and 150 µM | Reduction of LPS/TNF-induced TNF, IL-6, IL-8, MCP-1, MIP-2, and ICAM-1 |
Human HepG2 cells | 1, 5, and 10 µM | Reduction of H2O2-induced cellular oxidative stress; Increase of GSH, GCS, and ARE activity |
5 and 10 µM | Block of GST Upregulation of pJNK, Nrf2, and HO-1 |
|
Human THP-1 macrophages | 5 and 20 µM | Reduction of LPS/ATP-triggered IL-1β and secretion and mRNA; inhibition of NLRP3 and active caspase-1 |
Human HT29/B6 | 100 µM | Reduction of TNF-induced Akt, IκBα and NFκB phosphorylation; induction of ERK and p38 |
75, 100, and 125 µM | Increase of TER and prevention of fluorescein permeability and claudin 1, down-regulation of claudin 2 | |
Murine chondrogenic cell line ATDC5 | 5 µM | Reduction of LPS/IL-1β-induced NO, LPS-induced MCP-1, IL-6, MyD88, ERK phosphorylation and iNOS |
Human primary chondrocytes | 5 µM | Reduction of cathepsin K activity |
Primary rat astrocytes | 10 µM | Reduction LPS-triggered IL-1β and IL-6 release, iNOS and COX-2 protein, LPS-induced HDAC1 protein and up-regulation of HSP70; restoration of acetyl histone 3 protein after LPS degradation |