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$\gamma$

TNF-$\alpha$ 자극에 의한 U937 단핵구 세포의 HT29 대장 상피 세포 부착에 대한 Berberine의 PPAR$\gamma$가 아닌 NF-$\kappa$B 경로를 통한 억제 효과

  • Received : 2009.09.08
  • Accepted : 2009.10.20
  • Published : 2010.04.30

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

References

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