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KMID : 0043320160390101465
Archives of Pharmacal Research
2016 Volume.39 No. 10 p.1465 ~ p.1471
Isoliquiritigenin suppresses tumor necrosis factor-¥á-induced inflammation via peroxisome proliferator-activated receptor-¥ã in intestinal epithelial cells
Jin Xing Yu

Sohn Dong-Hwan
Lee Sung-Hee
Abstract
Intestinal epithelial cells play an important role in the mucosal immune reaction in inflammatory bowel diseases via the expression of inflammatory mediators, such as cyclooxygenase-2 (COX-2) and intercellular adhesion molecule-1 (ICAM-1). Isoliquiritigenin (ISL; 4,2¡Ç,4¡Ç-trihydroxychalcone) has been shown to exhibit anti-inflammatory properties in murine macrophage cells. In the present study, we evaluated the anti-inflammatory properties of ISL in intestinal epithelial cells and determined its mechanism of action. ISL suppressed the expression of COX-2 and ICAM-1 in tumor necrosis factor-¥á (TNF-¥á) stimulated intestinal epithelium HT-29 cells. It also induced peroxisome proliferator-activated receptor-¥ã (PPAR¥ã) protein expression. Moreover, using a PPAR¥ã antagonist, GW9662, we found that the regulation of COX-2 and ICAM-1 expression by ISL in TNF-¥á-stimulated HT-29 cells is mediated via PPAR¥ã expression. A signal transduction study revealed that ISL significantly attenuates TNF-¥á-mediated JNK phosphorylation. ISL-induced ERK1/2 phosphorylation was associated with PPAR¥ã expression. Additionally, both the inhibitory effect on COX-2 and ICAM-1 expression and the induction of PPAR¥ã expression by ISL in TNF-¥á-stimulated HT-29 cells was abolished by the addition of U0126, a specific ERK1/2 inhibitor. Collectively, ISL-induced PPAR¥ã mediated, at least partially, the suppression of intestinal inflammation. These results suggest that ISL may be beneficial for the treatment of mucosal inflammation.
KEYWORD
Isoliquiritigenin, Inflammatory bowel diseases, Intestinal epithelial cells, Tumor necrosis factor-¥á, Peroxisome proliferator-activated receptor-¥ã
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