Next Article in Journal
Potential Role of Sulfur-Containing Antioxidant Systems in Highly Oxidative Environments
Previous Article in Journal
Optimization of Supercritical Fluid Extraction of Oil from the Fruit of Gardenia jasminoides and Its Antidepressant Activity
Article Menu

Export Article

Open AccessArticle
Molecules 2014, 19(12), 19361-19375; doi:10.3390/molecules191219361

EOP, a Newly Synthesized Ethyl Pyruvate Derivative, Attenuates the Production of Inflammatory Mediators via p38, ERK and NF-κB Pathways in Lipopolysaccharide-Activated BV-2 Microglial Cells

1
Department of Biotechnology, College of Biomedical and Health Science, Konkuk University, Chungju 380-701, Korea
2
Department of Molecular Science and Technology, Ajou University, Suwon 443-749, Korea
3
Branch of Immune and Cell Therapy, National Cancer Center, Goyang 410-769, Korea
*
Author to whom correspondence should be addressed.
Received: 10 October 2014 / Revised: 3 November 2014 / Accepted: 18 November 2014 / Published: 25 November 2014
(This article belongs to the Section Medicinal Chemistry)
View Full-Text   |   Download PDF [1296 KB, uploaded 25 November 2014]   |  

Abstract

Microglia-induced neuroinflammation is an important pathological mechanism influencing various neurodegenerative disorders. Excess activation of microglia produces a myriad of proinflammatory mediators that decimate neurons. Hence, therapeutic strategies aimed to suppress the activation of microglia might lead to advancements in the treatment of neurodegenerative diseases. In this study, we synthesized a novel ethyl pyruvate derivative, named EOP (S-ethyl 2-oxopropanethioate) and studied its effects on lipopolysaccharide (LPS)-induced production of nitric oxide (NO) in rat primary microglia and mouse BV-2 microglia. EOP significantly decreased the production of NO, inducible nitric oxide synthase, cyclooxygenase and other proinflammatory cytokines, such as interleukin (IL)-6, IL-1β and tumor necrosis factor-α, in LPS-stimulated BV-2 microglia. The phosphorylation levels of extracellular regulated kinase, p38 mitogen-activated protein kinase, and nuclear translocation of NF-κB were also inhibited by EOP in LPS-activated BV-2 microglial cells. Overall, our observations indicate that EOP might be a promising therapeutic agent to diminish the development of neurodegenerative diseases associated with microglia activation. View Full-Text
Keywords: ethyl pyruvate derivative; lipopolysaccharide; microglia; neuroinflammation; neurodegenerative diseases; primary microglia ethyl pyruvate derivative; lipopolysaccharide; microglia; neuroinflammation; neurodegenerative diseases; primary microglia
Figures

Figure 1

This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. (CC BY 4.0).

Scifeed alert for new publications

Never miss any articles matching your research from any publisher
  • Get alerts for new papers matching your research
  • Find out the new papers from selected authors
  • Updated daily for 49'000+ journals and 6000+ publishers
  • Define your Scifeed now

SciFeed Share & Cite This Article

MDPI and ACS Style

Min, S.; More, S.V.; Park, J.-Y.; Jeon, S.-B.; Park, S.Y.; Park, E.-J.; Yoon, S.-H.; Choi, D.-K. EOP, a Newly Synthesized Ethyl Pyruvate Derivative, Attenuates the Production of Inflammatory Mediators via p38, ERK and NF-κB Pathways in Lipopolysaccharide-Activated BV-2 Microglial Cells. Molecules 2014, 19, 19361-19375.

Show more citation formats Show less citations formats

Related Articles

Article Metrics

Article Access Statistics

1

Comments

[Return to top]

Molecules EISSN 1420-3049 Published by MDPI AG, Basel, Switzerland RSS E-Mail Table of Contents Alert
Back to Top