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논문 기본 정보

자료유형
학술저널
저자정보
Park, Su-Young (College of Pharmacy, Yeungnam University) Neupane, Ganesh Prasad (College of Pharmacy, Yeungnam University) Lee, Sung Ok (Graduate School of East-West Medical Science, Kyung Hee University) Lee, Jong Suk (College of Pharmacy, Yeungnam University) Kim, Mi-Young (College of Pharmacy, Yeungnam University) Kim, Sun Yeou (College of Pharmacy, Gachon University) Park, Byung Chul (CJ Pharmaceutical Research Institute) Park, Young-Joon (CJ Pharmaceutical Research Institute) Kim, Jung-Ae (College of Pharmacy, Yeungnam University)
저널정보
대한약학회 Archives of pharmacal research : a publication of the Pharmaceutical Society of Korea Archives of pharmacal research : a publication of the Pharmaceutical Society of Korea 제37권 제2호
발행연도
2014.1
수록면
253 - 262 (10page)

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In inflammatory bowel disease (IBD), colon epithelial cells express a variety of inflammatory mediators, including chemokines, which perpetuate inflammatory response. In the current study, we report that water extract of Pogostemon cablin Bentham aerial parts (PCW), which has traditionally been used for treatment of the common cold and infectious disease, suppressed colon inflammation. Treatment with PCW resulted in effective inhibition of tumor necrosis factor (TNF)-${\alpha}$-induced adhesion of monocytes to HT-29 human colonic epithelial cells. In a trinitrobenzene sulfonic acid (TNBS)-induced rat model of IBD, PCW suppressed clinical signs of colitis, including weight loss, colon tissue myeloperoxidase activity, a marker for inflammatory cell infiltration, and cyclooxygenase-2 expression in a dose-dependent manner. In addition, PCW suppressed TNBS-induced mRNA expression of IL-8, MCP-1, and IL-6 in rat colon. The nuclear level of NF-${\kappa}B$ in TNBS-treated rat colon and NF-${\kappa}B$ luciferase reporter gene activity in TNF-${\alpha}$-treated HT-29 cells were significantly inhibited by PCW. Taken together, the results of this study suggest that PCW suppressed colon inflammation via suppression of NF-${\kappa}B$-dependent expression of pro-inflammatory cytokines.

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