Objective To observe the antitumor action of Wei Yi Ting granules (WYTG) and to explore its possible mechanism.Methods The inhibitory effect of WYTG and its different WYTG ingredient combinations on the growth of S180 tumor in mice was observed.Meanwhile,the effect of WYTG and its different ingredient combinations on the expression of P53 and PCAN during tumor development was studied by immunohistochemical method.Results WYTG had an obvious inhibitory effect on tumor growth and could reduce the positive cell number of P53 and PCAN,the difference being significant as compared with the blank control group(P 0.05).Conclusion WYTG,which has the actions of strengthening Qi,activating blood and removing toxicity,exerts an obvious inhibitory effect on tumor as compared with its ingredient combination of strengthening Qi and with that of strengthening Qi and removing toxicity.Its therapeutic mechanism may be related to the inhibition of the expression of P53 and PCAN and the influence on tumor-associated gene during the growth of tumor.

Recent work has revealed that large numbers of mitotic figures are present in adult hearts,which has implied that there should be some mechanism about nature repair of the adult heart.But the levels of natural repair are not high enough to retrieval the traumatic myocardium.As a new approach to improving the cardiac repair,stem-cell therapy provides an exciting and powerful treatment.We describe the background of natural repair,and summarize the current strategies in the application of stem-cell therapy to repair the traumatic myocardium.

BACKGROUND: Fish oil is one of mainly natural resources of n-3 fatty acids, which can inhibit cardiac allograft vasculopathy (CAV) and prolong the survival of cardiac allograft. But, the mechanism is unclear. Recent in vitro data suggested that n-3 fatty acids could inhibit the release of inflammatory transmitter by the activation of peroxisome proliferator-activated receptor-y (PPARy). OBJECTIVE: To test the hypothesis that n-3 fatty acids from fish oil ameliorates CAV development via activating PPARy. METHODS: A total of 6 Lewis rats and 18 Fisher344 rats were randomly selected as heart donors. An additional 24 Lewis rats were randomly and equally divided into 4 groups. In isograft group, heart transplantation was performed among Lewis rats, without any drug. In low-dose fish oil-treated group, F344→Lewis transplantation was performed. At 1 day following surgery, 0.03 mL/kg fish oil was treated by gavage for 8 weeks. In high-dose fish oil-treated group, F344→Lewis transplantation was conducted. At 1 day following surgery, 0.06 mL/kg fish oil was treated by gavage for 8 weeks. In control group, F344→Lawis transplantation was conducted. Cyclosporine A was administrated by gavage for 8 weeks. In the low-dose and high-dose fish oil-treated groups, cyclosporine A (1.5 mg/kg) was given daily by intramuscular injection for 2 weeks following surgery. CAV was evaluated by histological examination. Activity of nuclear factor (NF) k-B and PPARy was assessed in homogenate. Contents of monocyte chemoattractant protein-1 and interferon-inducible protein 10 were measured by enzyme-labeled immunosorbent assay (ELISA). Chemokine receptor CCR2 and CXCR3 expression was determined by real-time quantitative reverse transcription-polymerase chain reaction (RT-PCR). RESULTS AND CONCLUSION: All 24 receptor Lewis rats were survived following surgery. The donor heart could regularly beat at 8 weeks following transplantation. Compared with the isograft group, severe CAV was detected in the control group al 8 weeks. Compared with the control group, CAV was significantly relieved, the activity of PPARy was significantly elevated, the activity of NF k-B was significantly decreased, levels of intragraft monocyte chemoattractant protein-1 and interferon-inducible protein-10 were significantly reduced in the low-dose and high-dose fish oil-treated groups (P < 0.001, P < 0.05), especially in the high-dose fish oil-treated group (P < 0.05). There was no significant difference in expression of chemokine receptors CXCR3 in the low-dose and high-dose fish oil-treated groups and control group. Our results demonstrated that n-3 fatty acids from fish oil can attenuate CAV development, possibly through activating PPARy and subsequently inhibiting the NF-kB activation, the chemokines secretion and its receptor expression in a dose-dependent fashion in rat models.