The Effective Analysis for Blue Honeysuckle Extract in the Treatment of Hepatocellular Carcinoma.

To further determine how BHE affected the growth of HCC cells, the proportion of each cell cycle phase was explored in HCC cells by flow cytometry. Blue honeysuckle (Lonicera caerulea L.) is a species of bush that grows in eastern Russia. Blue honeysuckle extract (BHE) is rich in bioactive phytochemicals which can inhibit the proliferation of tumor cells. The mechanism underlying the anticancer activity of BHE in primary liver cancer is poorly understood. The purpose of this study was to evaluate the growth inhibition mechanism of bioactive substances from blue honeysuckle on hepatocellular carcinoma (HCC) cells and to explore its protein and gene targets. The compounds in BHE were determined by high-performance liquid chromatography (HPLC) and liquid chromatography-mass spectrometry (LC-MS). Cell counting kit-8 (CCK8) assay was used to evaluate the effects of BHE on HCC cell proliferation, and flow cytometry assay (FCA) was used to determine how BHE arrested the proportion of each cell cycle phase in HCC cells. Western blot (WB) was performed to determine the expression of cell cycle-related proteins in HCC cells treated with different concentrations of BHE. The xenograft tumor animal models were established by HCC cell implantation. The results showed that cyanidin-3-o-glucoside and cyanidin-3-o-sophoroside which are the main biologically active components were detected in BHE. BHE is highly effective in inhibiting the proliferation of HCC cells by arresting the HCC cell cycle in the G2/M phase. BHE also downregulated the expression of conventional or classical dendritic cells-2 (cDC2) and cyclin B1 by promoting the expression of myelin transcription factor 1 (MyT1) in HCC cells. The weight and volume of xenografts were significantly decreased in the BHE treated groups when compared to the control group. BHE increased the expression of MyT1 in xenograft tissues. These findings showed that blue honeysuckle extract inhibits proliferation in vivo and in vitro by downregulating the expression of cDC2 and cyclin B1 and upregulating the expression of MyT1 in HCC cells.

Anti-proliferative effect of an extract of the root of Polygonum multiflorum Thunb. on MCF-7 human breast cancer cells and the possible mechanisms.

The root of Polygonum multiflorum Thunb. (PM) is utilized to treat many diseases associated with aging. Research also indicates that PM inhibits the proliferation of certain types of cancer cells. The aim of the present study was to evaluate the inhibitory effect of PM extract (PME) on the proliferation of MCF-7 cells and to investigate the underlying mechanisms. Inhibition of the proliferation of MCF-7 cells was determined by the MTT assay. Cell cycle distribution and apoptotic rates were evaluated by flow cytometry, and cell cycle and apoptosis-related protein expression was assessed by Western blotting. Apoptotic characteristics of MCF-7 cells were detected by transmission electron microscopy. The present study showed that PME at doses of 100, 150, 200 and 250 µg/ml significantly inhibited proliferation of MCF-7 cells in a time- and dose-dependent manner. Flow cytometry showed that the cell apoptotic rates were 9.1 ± 1.67 and 17.7 ± 2.93% after treatment with 100 and 200 µg/ml PME for 48 h, respectively. The proportions of cells in the G2/M phase were 37.9 ± 1.47 and 42.0 ± 1.71% after treatment with 100 and 200 µg/ml PME for 24 h, respectively. Western blot analysis showed that PME down-regulated the protein expression of Cdc25B and Cdc25C phosphatases accompanied by an increase in phospho-Cdk1, and PME promoted cytochrome c release from mitochondria into the cytosol to activate caspase-9. The present study demonstrated that PME inhibited MCF-7 cell proliferation by inducing cell cycle arrest in the G2/M phase and promoting cell apoptosis. The effects of PME on MCF-7 cells were associated with the modulation of the expression levels of proteins involved in the cell cycle and apoptosis. These data suggest that PME has promise as a treatment against breast cancer by inhibiting the proliferation of cancer cells.

Effects of raspberry phytochemical extract on cell proliferation, apoptosis, and serum proteomics in a rat model.

The red raspberry extract possesses potent antioxidant capacity and anticancerous activity in vitro and in vivo. The objective of this study was to determine whether red raspberry extract affected the cell cycle, angiogenesis, and apoptosis in hepatic lesion tissues from a rat model induced by diethylnitrosamine (DEN) as well as changes of serum proteomics. Rats were treated with red raspberry extract (0.75, 1.5, or 3.0 g/kg of body weight) by gavage starting 2 h after DEN administration and continued for 20 wk. Red raspberry extract inhibited cell proliferation, vascular endothelial growth factor VEGF expression, and induced apoptosis in the hepatic lesion tissues. In addition, 2 protein peaks (2597.93 and 4513.88 m/z) were identified to differentially express in the 3.0 g/kg body weight and positive control groups by serum proteomics. These results suggest that a dietary supplement with red raspberry effectively protects against chemically induced hepatic lesions in rats.

Antiangiogenetic effects of 4 varieties of grapes in vitro.

The purpose of this study was to investigate the inhibitory effects of grapes on the human umbilical vein endothelial (HUVE) cells' capillary tube formation and matrix metalloproteinase-2 (MMP-2) expression secreted into the medium. Four different grape varieties (Concord, Niagara, Chardonnay, and Pinot Noir) were extracted using 80% acetone and the extracts were stored at -80 degrees C. The total amount of phenolics and flavonoids for each of the 4 grape varieties were determined by spectrophotometry. Grape extracts were co-cultured with HUVE cells on Matrigel and inhibitory effects on tube formation were observed under a microscope. The inhibitory effects of grape extracts on MMP-2 expression were examined by zymogram. All 4 grape varieties inhibited the tube formation of HUVE cells in a dose-dependent manner on Matrigel. Except for Chardonnay, the other 3 grape varieties completely inhibited secretion of MMP-2 at 20 mg/mL. There was a significant positive relationship between the total phenolics and flavonoids and antiangiogenetic activities. The grapes tested have the potential to inhibit angiogenesis mainly by their phenolics and flavonoids contents, which partly contribute to their cancer chemopreventive efficacy.

Cranberry phytochemical extract inhibits SGC-7901 cell growth and human tumor xenografts in Balb/c nu/nu mice.

Cranberry extract possesses potent antioxidant capacity and antiproliferative activity against cancer in vitro and in vivo. The objectives of this study were to determine whether the cranberry extract inhibited proliferation of human gastric cancer SGC-7901 cells and human gastric tumor xenografts in the Balb/c nu/nu mouse. Cranberry extract at doses of 0, 5, 10, 20, and 40 mg/mL significantly inhibited proliferation of SGC-7901 cells, and this suppression was partly attributed to decreased PCNA expression and apoptosis induction. In a human tumor xenograft model, the time of human gastric tumor xenografts in the mouse was delayed in a dose-dependent manner. A dose-response inhibition was also observed in the averages of size, weight, and volume of tumor xenografts in the mouse between the control and cranberry-treated groups. These results demonstrate fresh cranberries to be a chemopreventive reagent.