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Inhibitory Effect of Berberine on TNF-$\alpha$-induced U937 Monocytic Cell Adhesion to HT29 Human Colon Epithelial Cells is Mediated through NF-$\kappa$B Rather than PPAR$\gamma$  

Park, Su-Young (College of Pharmacy, Yeungnam University)
Lee, Gwang-Ik (College of Pharmacy, Yeungnam University)
Kim, Il-Yeob (College of Pharmacy, Yeungnam University)
Kim, Jung-Ae (College of Pharmacy, Yeungnam University)
Publication Information
YAKHAK HOEJI / v.54, no.2, 2010 , pp. 91-96 More about this Journal
Abstract
Berberine, an isoquinoline alkaloid, has a wide range of pharmacological effects, including anti-inflammation. It has been reported that berberine inhibits experimental colitis through inhibition of IL-8, and that inhibitory effect of berberine on inflammatory cytokine expression is mediated through peroxisome proliferator activated receptor (PPAR)-$\gamma$. In this study, we examined the effects and action mechanism of berberine on the tumor necrosis factor (TNF)-$\alpha$-induced monocyte adhesion to HT29 human colonic epithelial cells, which is commonly used as an in vitro model of inflammatory bowel disease (IBD). Berberine significantly inhibited the TNF-$\alpha$-induced monocyte adhesion to HT29, which is similar to the effect of PDTC, a nuclear factor (NF)-$\kappa$B inhibitor. However, ciglitazone and GW, the ligands of PPAR-$\gamma$, did not suppress the TNF-$\alpha$-induced monocyte adhesion to HT29 cells. In addition, TNF-$\alpha$-induced chemokine expression and NF-$\kappa$B transcriptional activity were significantly inhibited by berberine in a concentration-dependent manner. The results suggest that inhibitory effect of berberine on colitis is mediated through suppression of NF-$\kappa$B and NF-$\kappa$B-dependent chemokine expression.
Keywords
berberine; colitis; nuclear factor (NF)-$\kappa$B; peroxisome proliferator activated receptor (PPAR)-$\gamma$; chemokine;
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