|
KMID : 1140220180230030134
|
|
대한암예방학회지
2018 Volume.23 No. 3 p.134 ~ p.140
|
|
|
Diallyl Trisulfide Suppresses the Production of Lipopolysaccharide-induced Inflammatory Mediators in BV2 Microglia by Decreasing the NF-κB Pathway Activity Associated With Toll-like Receptor 4 and CXCL12/CXCR4 Pathway Blockade
|
|
Lee Hye-Hyeon
Jeong Jin-Woo
Hong Su-Hyun
Park Cheol
Kim Byung-Woo
Choi Yung-Hyun
|
|
|
Abstract
|
|
|
Background: Diallyl trisulfide (DATS), a garlic-derived organosulfuric compound, has been documented for potential anti-inflammatory effects. However, the mechanism in microglia remains unknown. In this study, we investigated the anti-inflammatory effects of DATS in lipopolysaccharide (LPS)-stimulated BV2 microglial cells.
Methods: The effects of DATS on LPS-induced pro-inflammatory mediators such as nitric oxide (NO) and prostaglandin E2 (PGE2) were assessed under conditions not in the cytotoxicity of DATS. The protein expression of inflammation regulatory genes was measured by Western blot analysis.
Results: DATS significantly inhibited the LPS-induced secretion of NO and PGE2, which was associated with the suppression of their regulatory genes, inducible NO synthase and COX-2. DATS had been shown to inhibit nuclear translocation of NF-κB by destroying the degradation and phosphorylation of IκB-α inhibitors in the cytoplasm. In addition, DATS effectively inhibited the expression of LPS-induced toll-like receptor 4 (TLR4) and myeloid differentiation factor 88. Furthermore, DATS markedly reduced the LPS-induced expression of chemokine (CXC motif) ligand (CXCL) 12 and CXC receptor (CXCR) 4, demonstrating its capacity to block chemo-attractive activity.
Conclusions: These results indicate that DATS inhibits the activation of the CXCL12/CXCR4 axis associated with antagonizing effect on TLR4 and blocks NF-κB signaling, thus demonstrating anti-inflammatory effects against LPS stimulation.
|
|
|
KEYWORD
|
|
|
Diallyl trisulfide, Anti-inflammation, NF-κB, Toll-like receptor 4, Chemokine
|
|
|
FullTexts / Linksout information
|
|
|
|
|
|
Listed journal information
|
|
 
|