Synergistic enhancement of the antitumor activity of 5-fluorouracil by bornyl acetate in SGC-7901 human gastric cancer cells and the determination of the underlying mechanism of action.

PURPOSE: To investigate the anticancer activity of bornyl acetate and its combination with low dose 5-fluorouracil (5-FU) in human gastric cancer (SGC-7901) cells and to evaluate their effects on cell cycle, apoptosis, cancer cell morphology and DNA fragmentation. METHODS: The anticancer activity of bornyl acetate, 5-FU and their combination against human gastric cancer (SGC-7901) cells was evaluated by MTT assay. Flow cytometry using propidium iodide (PI) as a staining agent was used to study the effect of the extract on cell cycle phase distribution. Apoptosis induced by bornyl acetate and 5-FU was evaluated by Annexin V binding assay using flow cytometer. Alterations in cell morphology following apoptosis was studied by fluorescence microscopy as well as transmission electron microscopy. RESULTS: Bornyl acetate induced dose-dependent growth inhibitory effects on human gastric cancer cells in vitro.The combination of bornyl acetate with 5-FU induced a much more growth inhibitory effect on these cells indicating a synergistic enhancement of anticancer activity of 5-FU. The combined effect of bornyl acetate and 5-FU also resulted in greater apoptosis induction as well as cell cycle arrest in comparison to the individual treatment by bornyl acetate or 5-FU. Fluorescence microscopy as well as transmission electron microscopy also revealed that the combination of bornyl acetate with 5-FU resulted in greater apoptosis induction as well as cell morphology alterations. The percentages of early as well as late apoptotic cells were much higher in the combination treatment in comparison to separate treatment by bornyl acetate or 5-FU. CONCLUSION: Bornyl acetate potentiates the anticancer activity of 5-FU in human gastric cancer (SGC-7901) cells by inducing apoptosis, DNA fragmentation as well as G2/M cell cycle arrest.

Effects of psychological stress on small intestinal motility and bacteria and mucosa in mice.

AIM: To investigate the effects of psychological stress on small intestinal motility and bacteria and mucosa in mice, and to explore the relationship between small intestinal dysfunction and small intestinal motility and bacteria and mucosa under psychological stress. METHODS: Sixty mice were randomly divided into psychological stress group and control group. Each group were subdivided into small intestinal motility group (n = 10), bacteria group (n = 10), and D-xylose administered to stomach group (n = 10). An animal model with psychological stress was established housing the mice with a hungry cat in separate layers of a two-layer cage. A semi-solid colored marker (carbon-ink) was used for monitoring small intestinal transit. The proximal small intestine was harvested under sterile condition and processed for quantitation for aerobes (Escherichia coli) and anaerobes (Lactobacilli). The quantitation of bacteria was expressed as log10(colony forming units/g). D-xylose levels in plasma were measured for estimating the damage of small intestinal mucosa. RESULTS: Small intestinal transit was inhibited (39.80+/-9.50% vs 58.79+/-11.47%, P<0.01) in mice after psychological stress, compared with the controls. Psychological stress resulted in quantitative alterations in the aerobes (E. coli). There was an increase in the number of E. coli in the proximal small intestinal flora (1.78+/-0.30 log10 (CFU/g) vs 1.37+/-0.21 log10 (CFU/g), P<0.01), and there was decrease in relative proportion of Lactobacilli and E. coli of stressed mice (0.53+/-0.63 vs 1.14+/-1.07, P<0.05), while there was no significant difference in the anaerobes (Lactobacilli) between the two groups (2.31+/-0.70 log10 (CFU/g) vs 2.44+/-0.37 log10 (CFU/g), P>0.05). D-xylose concentrations in plasma in psychological stress mice were significantly higher than those in the control group (2.90+/-0.89 mmol/L vs 0.97+/-0.33 mmol/L, P<0.01). CONCLUSION: Small intestinal dysfunction under psychological stress may be related to the small intestinal motility disorder and dysbacteriosis and the damage of mucosa probably caused by psychological stress.