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This study investigated the mechanism of the cytotoxic effect of emodin, an active anthraquinone, on human lung adenocarcinoma A549 cells. In vitro growth inhibition and suppression on colony forming were used to evaluate the effects of emodin on A549 cells. Emodin's ability in changing the expressions of apoptosis-related genes was studied by real-time RT-PCR. Emodin could significantly inhibit the growth of A549 cells with IC50 = 16.85 μg/ml (~60 μM). It also concentration dependently inhibited the colony-forming ability of A549 cells with IC50 = 7.60 μg/ml (~30 μM). Hallmarks of apoptosis, such as single-strand DNA breakage and DNA fragmentation, were observed in A549 cells treated with emodin. Emodin (72 h) treatment could up-regulate the gene expression of FASL (p < 0.05) and down-regulate the gene expression of C-MYC (p < 0.01), but induce no significant changes in the gene expressions of MCL1, GAPDH, BAX and CCND1. These results suggest that emodin could induce growth inhibition and apoptosis in A549 cells through modifying the extrinsic apoptotic pathways and the induction of cell cycle arrest.

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An integrated approach including chemical and biological assessments was developed to investigate the differences between Apocynum venetum L. (AV) and its adulterant, Apocynum pictum Schrenk (AP). Ten flavonoids were tentatively identified by ultra-visible and mass spectra data. The chemical component, hyperoside, was identified as a critical parameter for discrimination of two species from the results of principal component analysis (PCA) and quantitative analysis. The anti-oxidative power of the herbal extracts were determined using 2,2-diphenyl-1-(2,4,6-trinitrophenyl) hydrazyl (DPPH) assay and H2O2-induced cell damage on LO2 cells. The results of the biological assays suggested that the chemical differences between AV and AP do lead to difference in activity and AV is demonstrated to have higher anti-oxidant activity.

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