J Cancer Prev.
2018 Sep;23(3):134-140. 10.15430/JCP.2018.23.3.134.
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
- Affiliations
-
- 1Anti-Aging Research Center and Blue Bio Industry RIC, Dong-Eui University, Busan, Korea. choiyh@deu.ac.kr
- 2Freshwater Bioresources Utilization Bureau, Nakdonggang National Institute of Biological Resources, Sangju, Korea.
- 3Department of Biochemistry, Dong-Eui University College of Korean Medicine, Busan, Korea.
- 4Department of Molecular Biology, College of Natural Sciences, Dong-Eui University, Busan, Korea.
- 5Department of Life Science and Biotechnology, College of Engineering, Dong-Eui University, Busan, Korea.
- KMID: 2425316
- DOI: http://doi.org/10.15430/JCP.2018.23.3.134
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.
MeSH Terms
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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*
Dinoprostone
Myeloid Differentiation Factor 88
Nitric Oxide
Nitric Oxide Synthase
Toll-Like Receptor 4
Toll-Like Receptors
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