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Effects of Aralia continentalis Root Extract on Cell Proliferation and Apoptosis in Human Promyelocytic Leukemia HL-60 Cells
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  • Effects of Aralia continentalis Root Extract on Cell Proliferation and Apoptosis in Human Promyelocytic Leukemia HL-60 Cells
  • Effects of Aralia continentalis Root Extract on Cell Proliferation and Apoptosis in Human Promyelocytic Leukemia HL-60 Cells
저자명
Lim. Hae-Young,Oh. Ha-Lim,Lee. Chul-Hoon
간행물명
Journal of microbiology and biotechnology
권/호정보
2006년|16권 9호|pp.1399-1404 (6 pages)
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한국미생물생명공학회
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정기간행물|ENG|
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이 논문은 한국과학기술정보연구원과 논문 연계를 통해 무료로 제공되는 원문입니다.
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The roots of Aralia continentalis (AC) have been used traditionally in Korean as a folk medicine for anti-inflammation and as an anti-rheumatic. In this study, we report that the ethyl acetate-soluble traction (ACE) of the methanolic extract of AC root inhibited the cell growth of various human cancer cell lines and induced apoptosis of HL-60, human promyelocytic leukemia cells. Its $IC_{50}$ values on growth inhibition were estimated to be $56.3{mu}g/ml$ on HL-60, $87.2{mu}g/ml$ on HepG2, $93.2{mu}g/ml$ on HeLa, $135.5{mu}g/ml$ on DU-145, and $135.8{mu}g/ml$ on HT-29 cells. Interestingly, ACE showed no antiproliferative effect on normal lymphocyte cells used as control. Furthermore, nuclear DAPI staining revealed the typical nuclear features of apoptosis in the HL-60 cells exposed to $80{mu}g/ml$ ACE, and a flow cytometric analysis of the HL-60 cells using propidium iodide showed that the apoptotic cell population increased gradually from 5% at 0 h to 16% at 12 h and 20% at 24 h after treated with $50{mu}g/ml$ of ACE. TUNEL assay also revealed the apoptotic induction of the HL-60 cells treated with ACE. To obtain further information on the ACE-induced apoptosis, the expression level of certain apoptosis-associated proteins was examined using a Western blot analysis. Treatment of the HL-60 cells with ACE resulted in the activation of caspase-3, and subsequent proteolytic cleavage of poly(ADP-ribose) polymerase (PARP). The above results confirmed that the apoptosis in the HL-60 cells was induced by ACE, and that caspase-3-mediated PARP cleavage was involved in the process.