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
10.15430/JCP.2018.23.3.134
- Author:
Hye Hyeon LEE
1
;
Jin Woo JEONG
;
Su Hyun HONG
;
Cheol PARK
;
Byung Woo KIM
;
Yung Hyun CHOI
Author Information
1. Anti-Aging Research Center and Blue Bio Industry RIC, Dong-Eui University, Busan, Korea. choiyh@deu.ac.kr
- Publication Type:Original Article
- Keywords:
Diallyl trisulfide;
Anti-inflammation;
NF-κB;
Toll-like receptor 4;
Chemokine
- MeSH:
Blotting, Western;
Cytoplasm;
Dinoprostone;
Genes, Regulator;
Inflammation;
Microglia;
Myeloid Differentiation Factor 88;
Nitric Oxide;
Nitric Oxide Synthase;
Phosphorylation;
Toll-Like Receptor 4;
Toll-Like Receptors
- From:Journal of Cancer Prevention
2018;23(3):134-140
- CountryRepublic of Korea
- Language:English
-
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.
