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TNF-α 자극에 의한 U937 단핵구 세포의 HT29 대장 상피 세포 부착에 대한 Berberine의 PPARγ가 아닌 NF-κB 경로를 통한 억제 효과
박수영(Su-Young Park),이광익(Gwang Ik Lee),김일엽(Il-Yeob Kim),김정애(Jung-Ae Kim) 대한약학회 2010 약학회지 Vol.54 No.2
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)-γ. In this study, we examined the effects and action mechanism of berberine on the tumor necrosis factor (TNF)-α-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-α-induced monocyte adhesion to HT29, which is similar to the effect of PDTC, a nuclear factor (NF)-κB inhibitor. However, ciglitazone and GW, the ligands of PPAR-γ, did not suppress the TNF-α-induced monocyte adhesion to HT29 cells. In addition, TNF-α-induced chemokine expression and NF-κB 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-κB and NF-κB-dependent chemokine expression.