Effect of the silencing of TNF alpha and glycine receptors on the secretion of pro-inflammatory cytokines in 3T3-L1 preadipocytes
Obesity has been related to a process of chronic inflammation, which is characterized by an increase in pro-inflammatory cytokine levels. It has been reported that glycine decreases the secretion of TNF alpha and IL-6 in adipocytes, although the mechanisms have not yet been clarified. The purpose of...
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Published in | Proceedings for Annual Meeting of The Japanese Pharmacological Society Vol. WCP2018; p. PO3-6-26 |
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Main Authors | , , , , , , , |
Format | Journal Article |
Language | English |
Published |
Japanese Pharmacological Society
2018
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Subjects | |
Online Access | Get full text |
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Summary: | Obesity has been related to a process of chronic inflammation, which is characterized by an increase in pro-inflammatory cytokine levels. It has been reported that glycine decreases the secretion of TNF alpha and IL-6 in adipocytes, although the mechanisms have not yet been clarified. The purpose of this study was to determine the mechanism by which glycine reduces the secretion of TNF alpha and IL-6 using siRNA from the TNF alpha and glycine receptors.METHODS: Several types of glycine receptors were characterized by RT-PCR. 3T3-L1 cells were transfected with siRNA for glycine receptor; three days later, the cells were ready for the experiments. 3T3-L1 cells was treated with Glycine 10 mM. Total RNA was extracted from the cells for the determination of TNF alpha and IL-6 expression by RT-PCR; in addition, the concentration of these cytokines in the medium was quantified by ELISA. RESULTS: Glycine decreased the production and release of TNF alpha and IL-6, whereas treatment with siRNA for the TNF alpha and glycine receptors produced increases in the secretion of the levels of these cytokines.CONCLUSION: These findings give clues about the signaling mechanisms by which glycine inhibits the secretion of pro-inflammatory adipokines in obesity. |
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Bibliography: | WCP2018_PO3-6-26 |
ISSN: | 2435-4953 2435-4953 |
DOI: | 10.1254/jpssuppl.WCP2018.0_PO3-6-26 |