Fuzheng Yiliu Keli Tumor Immunity Function Cell Cycle Apoptotic Rate Calcium In Cell Apoptosis Gene Modulation

1 ObjectiveTo explore the anti-tumor effect and mechanism of Fuzheng Yiliu keli(FYK) through animal experiment and clinical observation.2 Methods:In animal experiment the models of ascites tumor and solid tumor were developed by H22 tumor transplantation in Kunming mice. The animal model was divided into larger FYK dose group, smaller FYK dose group, Tianxian Capsule group (positive control) and bear ing tumor model group (negative control). In each group the drug was administrated by gastrogavage at the same volume. Tumor-inhibiting-rate was calculated by the tumor weight in mice, meanwhile life elongation rate was calculated by the median survival rate of mice. NF-KB, cell cycle and apoptotic rate were determined by Flow Cytometer; The change of free intracellular Ca2+ concentration was detected by Confocal Laser Scanning Microscope; The expression of p53, Bcl-2 in tumor tissue and Fas/FasL in peripheral blood were observed by FCM. In clinical research, esophageal carcinoma patients and mammary adenocarcinoma patients were employed. T cell subset , NK , NF-KB, cell cycle and apoptotic rate were determined by FCM. The viscosity of the whole blood was measured by blood rheometer.3 ResultsAnimal experiments showed: (1) There were significant differences of tumor-inhibit ing-rate and life elongation rate between FYK group and model group. The effect of FYK was most excellent in the larger one. The rate was 51. 72% and 51. 61% respectively. (2) The proportion of G0/1 phase cell in model group was the lowest, whereas the proportion of S phase cell was the highest. The proportion of G0/1 phase cell rose and the proportion of S phase cell fell after treatment. The rate of the expression of NF-KB in larger FYK dose group was 26. 51%. Compared with model group, there was significant difference (P<0. 001). (3)There were significant difference of the concentration of [Ca2+]i and the apoptotic rate between the drugs and control group. (4) Between the drugs and the control, the expression of Fas of T lymphocyte in the peripheral blood fell apparently, whereas the expression of FasL rose apparently. (5) Compared with the control, the expression of p53 of tumor cell rose and the expression of Bcl-2 fell in the drugs group.In clinic research it showed: (1) In esophageal carcinoma patients, CD4, CD8, CD4/CD8 and NK cells in the drug groups were higher than in the control (P<0. 05), whereas the viscosity of the whole blood in the drug groups was lower than in the control (P<0. 05). Compared with the control, the quantity of leucocytes in chemotherapy group combined with FYK were more than in the single drugs. (2) The expression of NF-KB, the ratio of G0/1 phase and the rate of apoptosis in tested group with esophagus carcinoma improved, while the ratio of S phase was opposite (P<0. 05). (3) For those mammary adenocarcinoma patients, the level of CD4, CD8, CD4/CD8 and NK cells were also higher than that of the control (P<0. 05), while the whole blood stagnation descended obviously (P <0. 005). (4) The expression of NF-KB, the ratio of G0/1 phase increased (P<0. 01), whereas the ratio of S phase and the cell proliferation index (PI) decreased (P <0. 01). 4 ConclusionsFYK plays an important role in anti-tumor effect, especially in larger FYK dose group. The mechanisms maybe associated with several aspects. It can play a positive role to improve immunity, whereby inhibit activating AICD (activation-induced cell death); It can reduce the viscosity of the whole blood; It may exert influence on the transcripts of the Gene associated with proliferation and apoptosis of tumor cell; It has the effect of disturbing cell cycle. It can adjust the conduction of cell ion signals. It can improve apoptosis of tumor cell.