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자료유형
학술저널
저자정보
Park, Mi-Kyung (Laboratory of Chemical Genomics, Pharmacology Research Center, Korea Research Institute of Chemical Technology) Cheon, Myeong-Sook (Center of Herbal Resources Research, Korea Institute of Oriental Medicine) Kim, Seong-Hwan (Laboratory of Chemical Genomics, Pharmacology Research Center, Korea Research Institute of Chemical Technology) Chun, Jin-Mi (Center of Herbal Resources Research, Korea Institute of Oriental Medicine) Lee, A-Yeong (Center of Herbal Resources Research, Korea Institute of Oriental Medicine) Moon, Byeong-Cheol (Center of Herbal Resources Research, Korea Institute of Oriental Medicine) Yoon, Tae-Sook (Center of Herbal Resources Research, Korea Institute of Oriental Medicine) Choo, Byung-Kil (Department of Crop Agriculture & Life Science, College of Agriculture & Life Science, Chonbuk National University) Kim, Ho-Kyoung (Center of Herbal Resources Research, Korea Institute of Oriental Medicine)
저널정보
한국응용생명화학회 Applied Biological Chemistry Applied Biological Chemistry 제54권 제2호
발행연도
2011.1
수록면
188 - 193 (6page)

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Asparagus cochinchinensis Merrill (Liliaceae) has been traditionally used for the treatment of cancer in Korea and China, but its anticancer activity and underlying mechanism remain to be defined. Anticancer activities were investigated on fractions obtained from A. cochinchinensis 70% ethanol extract (ACE-EtOH) in human hepatocellular carcinoma HepG2 cells. Ethylacetate fraction from A. cochinchinensis extract (ACE-EA), more effective than other fractions, induced apoptosis of HepG2 ($IC_{50}=72.33{\pm}0.34{\mu}g/mL$), as revealed by apoptotic feature observation, increased capase-3 activity and Poly ADP ribose polymerase cleavage, and decreased expression of X-linked inhibitor of apoptosis protein in a dose-dependent manner. Protein levels of autophagy-related molecules, microtubule-associated protein 1 light chain 3 ${\alpha}$ and beclin 1, appeared to be induced by ACE-EA, suggesting ACE-EA exhibits anti-cancer activity with induction via both apoptosis and autophagy signaling pathways in HepG2 cells.

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