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<heading id="D0DBE918FF97FF84FC91D26AFB8D347E" bold="true" box="[818,1101,1331,1350]" fontSize="36" level="1" pageId="3" pageNumber="4" reason="1">
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5.3.1.
<taxonomicName id="4C2C25F7FF97FF84FCD1D26AFB8D347E" ID-CoL="4C9K7" authority="C. A. Mey" authorityName="C. A. Mey" box="[882,1101,1331,1350]" class="Magnoliopsida" family="Araliaceae" genus="Panax" kingdom="Plantae" order="Apiales" pageId="3" pageNumber="4" phylum="Tracheophyta" rank="species" species="ginseng">Panax ginseng C.A. Mey</taxonomicName>
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Polysaccharides from
<taxonomicName id="4C2C25F7FF97FF84FB82D216FBB9345A" box="[1057,1145,1359,1378]" class="Magnoliopsida" family="Araliaceae" genus="Panax" kingdom="Plantae" order="Apiales" pageId="3" pageNumber="4" phylum="Tracheophyta" rank="species" species="ginseng">
<emphasis id="B9588266FF97FF84FB82D216FBB9345A" bold="true" box="[1057,1145,1359,1378]" italics="true" pageId="3" pageNumber="4">P. ginseng</emphasis>
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, among the most widely known and used medicinal plant, have been already shown promising anti-proliferative effects against several cancer cell lines (
<bibRefCitation id="EFBD2385FF97FF84FAA9D2DEFAAA34A2" author="Sun, X. Y." box="[1290,1386,1415,1434]" pageId="3" pageNumber="4" pagination="490 - 499" refId="ref13109" refString="Sun, X. Y., 2011. Structure and biological activities of the polysaccharides from leaves, roots, and fruits of Panax ginseng C. A. Meyer: an overview. Carbohydr. Polym. 85, 490 - 499." type="journal article" year="2011">Sun, 2011</bibRefCitation>
). In 2017, Liao and coworkers synthesized a Se-P deriving from an aqueous extract of ginseng roots obtaining a Se content of
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/g. The growth inhibitory effects of this Se-P were first investigated
<emphasis id="B9588266FF97FF84FAAFD283FA8B34D5" bold="true" box="[1292,1355,1498,1517]" italics="true" pageId="3" pageNumber="4">in vitro</emphasis>
using the HL-60 (human leukemia) cell line. Cells were incubated for 2472 h with increasing concentrations of the Se-P in the range 25400 μg/mL. The best results have been obtained after 48 h with applied doses of 50 μg/ mL, 100 μg/mL, and 200 μg/mL leading to a reduction of surviving cells in the range 34.2%53.6%. These concentration levels were then selected to perform further tests. The next parameter evaluated was the release of LDH, well established to be a signal of apoptotic induction and progress. The administration of Se-P provided a dose-dependent increase of LDH release. HL-60 cells were also morphologically examined. The group treated with the Se-P at 200 μg/mL was characterized by cell shrinkage, condensed nuclei, and fragmented cell membranes. Furthermore, the induction of apoptosis occurred at a mithochondrial level with changes in the
<emphasis id="B9588266FF97FF84FB77D01CFAC03660" bold="true" box="[1236,1280,1861,1880]" italics="true" pageId="3" pageNumber="4">trans</emphasis>
-membrane potential, activation of pro-caspase 9, in turn leading to cleavage of caspase 9, caspase 3, and PARP, to a dose-dependent increase of the expression of the pro-apoptotic protein Bax and in the mean time a decrease of the anti-apoptotic factor Bcl-2.
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