This study was performed to elucidate the anticancer mechanism of a lipid-soluble ginseng extract (LSGE) by analyzing induction of apoptosis and arrest of cell cycle progression using the NCI-H460 human lung cancer cell line. Proliferation of NCI-H460 cells was potently inhibited by LSGE in a dose-dependent manner. The cell cycle arrest at the G0/G1 phase in NCI-H460 cells was induced by LSGE. The percentage of G0/G1 phase cells significantly increased, while that of S phase cells decreased after treatment with LSGE. The expression levels of cyclin-dependent kinase2 (CDK2), CDK4, CDK6, cyclin D3 and cyclin E related to G0/G1 cells progression were also altered by LSGE. In addition, LSGE-induced cell death occurred through apoptosis, which was accompanied by increasing the activity of caspases including caspase-8, caspase-9 and caspase-3. Consistent with enhancement of caspase activity, LSGE increased protein levels of cleaved caspase-3, caspase-8, caspase-9, and poly-ADP-ribose polymerase (PARP). These apoptotic effects of LSGE were inhibited by the pan-caspase inhibitor Z-VAD-fmk. These findings indicate that LSGE inhibits NCI-H460 human lung cancer cell growth by cell cycle arrest at the G0/G1 phase and induction of caspase-mediated apoptosis.

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In vitro antioxidant potential of 30% (v/v) ethanolic extracts from Panax ginseng and Panax notoginseng roots was investigated. The polyphenol contents of Panax ginseng and Panax notoginseng extracts were 10.3±0.3 and 10.4±0.4 mg/gextract, respectively. The extracts of Panax ginseng and Panax notoginseng possessed an antioxidant potential in a concentrationdependent manner. EC 50 values of Panax ginseng and Panaxnotoginseng extracts for cation radical, reducing power, and nitrite were 4.76±0.12 and 6.24±0.14 mg/mL, 1.99±0.01 and 3.13±0.05 mg/mL, and 4.78±0.31 and 3.52±0.10 mg/mL, respectively.