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http://dx.doi.org/10.7778/jpkm.2014.28.3.047

Anti-inflammatory Activities of GyejigaChulBuTang on Lipopolysaccharide-stimulated RAW264.7 Cells  

Jeong, Min-Jeong (Department of Korean Pediatrics, College of Korean Medicine, Woosuk University)
Lee, Seung-Yeon (Department of Korean Pediatrics, College of Korean Medicine, Dongeui University)
Yu, Sun-Ae (Department of Korean Pediatrics, College of Korean Medicine, Dongeui University)
Kang, Kyung-Hwa (Department of Physiology, College of Korean Medicine, Dongeui University)
Publication Information
The Journal of Pediatrics of Korean Medicine / v.28, no.3, 2014 , pp. 47-58 More about this Journal
Abstract
Objectives GyejigaChulBuTang (GCBT) is a prescription used to treat acute and chronic arthritis in Korea, China, and Japan. This study assessed the anti-inflammatory and anti-oxidant activities of GCBT on lipopolysaccharide (LPS)-stimulated RAW264.7 macrophage cells. Methods Raw264.7 cells were pretreated with or without GCBT for 1 hour prior to incubation with LPS. Anti-inflammatory activity of GCBT was evaluated with reference to gene expression and production levels of proinflammatory cytokines ($TNF{\alpha}$, IL-$1{\beta}$, IL-6, GM-CSF and $INF{\gamma}$) and inflammatory mediators (iNOS, COX-2, NO and $PGE_2$). In addition, intracellular ROS generation and signal transduction of MAPK family, PI3K/Akt and $I{\kappa}B{\alpha}/NF{\kappa}B$ was investigated. Results Prior treatment with GCBT inhibited elevation of $TNF{\alpha}$, IL-$1{\beta}$, IL-6, GM-CSF, $INF{\gamma}$, NO and $PGE_2$, together with their cognate mRNAs in a dose-dependent manner. Intracellular ROS contents were similarly reduced. These effects were due to inhibition of LPS-induced phosphorylation of MAPK family, PI3K/Akt and $I{\kappa}B{\alpha}$ as well as nuclear translocation of $NF{\kappa}B$. Conclusions GCBT suppresses pro-inflammatory mediators. GCBT has potential in the treatment of juvenile rheumatoid arthritis associated with inflammation.
Keywords
GyejigaChulBuTang; RAW264.7 cells; Proinflammatory cytokine; Juvenile rheumatoid arthritis; Inflammation;
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