This suggests that the water extract of Da Huang exerts potential anticancer activity through growth inhibition and apoptosis on MCF-7 and A549 cells lines.
Lobeliae chinensis Herba (''ban bian lian''), Rheum officinale Baill. (''da huang''), Sanguisorba officinalis Linn. (''di yu''), Agrimonia pilosa Ledeb. (''xian he cao''), and Paris polyphylla Smith (''zhi hua tou'') are well-known traditional Chinese medicines. They are commonly used in traditional Chinese medicine formulae against cancer. In this study, the antioxidant and anticancer effects of water extracts of these herbs were investigated. In the antioxidant and anticancer studies, water extracts of di yu, xian he cao, and da huang were show to be the most antioxidative and had the highest growth inhibitory effect on human lung adenocarcinoma A549 cell and human breast cancer MCF-7 cell. By comparing their percentage free radical scavenging capacity (SR%) and percentage growth inhibition on A549 and MCF-7 cells, a positive linear relationship between antioxidant activity and anticancer effect of the five herbal water extracts was found. This suggested that the antioxidants of the herbal water extracts might contribute to their anticancer effects on A549 and MCF-7 cells.
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.
Context: The poor prognostic outcome of breast cancer is largely due to its resistance to cancer therapies. Development of therapeutic agents that can inhibit growth and induce apoptosis in breast cancer cells can help solve the problem. Emodin is an active anthraquinone that has been reported to have diverse biological effects. Objective: In this study, the anticancer effects of emodin on growth inhibition, apoptosis induction and the expression of apoptosis-related genes in MCF-7 cells were investigated. Materials and methods: Growth inhibition induced by emodin was investigated by the MTS assay and the colony formation assay; while emodin-induced apoptosis was determined by the COMET assay and DNA fragmentation detection. Emodin (35 mM)-induced alterations in the expression of apoptotic-related genes were detected by using real-time PCR. Results: Emodin had significant growth inhibitory effects on MCF-7 cells with IC 50 ¼ 7.22 mg/ml ($30 mM). It also exerted a concentration-dependant inhibitory effect on the colony-forming ability of MCF-7 cells with IC 50 ¼ 7.60 mg/ml ($30 mM). Hallmarks of apoptosis, such as singlestrand DNA breakage and DNA fragmentation, were observed in emodin-treated MCF-7 cells. The gene expression of Fas ligand (FASL) was up-regulated (p50.01) but those of MCL1, CCND1 and C-MYC were down-regulated (p50.05) in emodin-treated MCF-7 cells. Discussion and conclusion: This study indicated that emodin could induce growth inhibition and apoptosis in MCF-7 cells through the modulation of the expression of apoptosis-related genes. The growth inhibitory effects of emodin might involve both the intrinsic and the extrinsic apoptotic pathways and cell cycle arrest.
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