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Pioglitazone Suppresses Inflammatory Response in C6 Glial Cells via Modulating NF-κB Related Pathway

초록

영어

Peroxisome proliferator-activated receptors (PPARs) are ligand-activated nuclear receptors having three isoforms such as PPAR alpha, PPAR delta/beta, and PPAR gamma. PPARγ ligands have recently shown to down-regulate the inflammation associated with various neurodegenerative diseases. Therefore, this study investigated the anti-inflammatory effects
of pioglitazone, a synthetic agonist of PPARγ, on lipopolysaccharide (LPS)-stimulated C6 glial cells. Pioglitazone attenuated the expression of mRNAs and proteins of several cytokines including interleukin (IL)-1 β, IL6 and tumor necrosis factor (TNF)-α in dose-dependent manner.
However, treatment with PPARγ antagonist abolished the inhibitory effect of pioglitazone on cytokines expression, suggesting that proinflammatory cytokines expression can be regulated through interaction with PPARγ in C6 glial cells. In addition, pioglitazone significantly inhibited IκBα phosphorylation and degradation and completely blocked nuclear factor-κB (NF-κB) DNA binding. These results suggest that pioglitazone suppresses the LPS-induced inflammatory response in C6 glial cells by blocking IκBα/NF-κB pathway.

저자정보

  • Hong Sung CHUN Dept. of Biotechnology, Chosun University, Gwangju 501-759, Korea.

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