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논문 기본 정보

자료유형
학술저널
저자정보
Lee, Kyung-Jin (Department of Pharmacy, College of Pharmacy) Kim, Ji-Young (Department of Pharmacy, College of Pharmacy, Research Center for Proteineous Materials Chosun University) Jung, Kyung-Sik (Department of Pharmacy, College of Pharmacy, Research Center for Proteineous Materials Chosun University) Choi, Chul-Yung (Division of Food Science, Chinju International University) Chung, Young-Chul (Division of Food Science, Chinju International University) Kim, Dong-Hee (Department of Pathology, College of Oriental Medicine, Daejeon University) Jeong , Hye-Gwang (Department of Pharmacy, College of Pharmacy, Research Center for Proteineous Materials Chosun 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 제27권 제12호
발행연도
2004.1
수록면
1,238 - 1,244 (7page)

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The suppressive effects of Platycodi Radix (Changkil: CK), the root of Platycodon grandiflorum A. DC (Campanulaceae), on the progress of acute carbon tetrachloride $(CCl_4)$-induced hepatic fibrosis were investigated in the rat. CK significantly suppressed $(CCl_4)$-induced hepatic necrosis and inflammation, as determined by the serum enzymatic activities of alanine and aspartate aminotransferase and serum tumor necrosis factor-${\alpha}$ levels, in dose-dependent manners. In addition, the increased hepatic fibrosis after acute $(CCl_4)$ treatment was suppressed by the administration of CK. CK also significantly prevented the elevation of hepatic ${\alpha}$ 1(I) procollagen (type I collagen) mRNA and ${\alpha}$ -smooth muscle actin (${\alpha}$ -SMA) expressions in the liver of $(CCl_4)$-intoxicated rats and also suppressed the induction of ${\alpha}$ -SMA and type I collagen in cultured hepatic stellate cells, in dose-dependent manners. These results suggest that the suppressive effects of CK against the progress of acute $(CCl_4)$-induced hepatic fibrosis possibly involve mechanisms related to its ability to block both hepatic inflammation and the activation of hepatic stellate cells.

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