Objective To investigate the inhibitory effect of genistein on the invasion of ovarian carcinoma cell line SKOV 3 in vivo and in vitro. Methods The abilities of the genistein-treated SKOV 3 cells to invade through reconstituted matrigel in transwell chambers were investigated in vitro and the invasion effect in vivo was determined using the xenograft models of SKOV 3 in nude mice. Results The ability of the 20 ?mol/L genistein-treated cells to invade the reconstituted basement membrane was decreased significantly at 72 h. This inhibition was in a dose-dependent manner. Genistein at the dose of 40 ?mol/L had the strongest effect. The results in vivo suggested that the grade of invasion in control SKOV 3 cells was in a time-dependent manner and genistein-treated group could apparently inhibit the progress of invasion, localizing the tumor in invasion grade 0 or grade I, and decreasing the proportion of grades Ⅱ, Ⅲ, Ⅳ. Conclusion The results suggest that genistein has inhibitory effect on the invasion of human ovarian carcinoma cell lines SKOV 3 in vivo and in vitro.

Objective To investigate how genistein to inhibit the invasion of human ovarian serous papillary cystadenocarcinoma cell line SKOV3.Methods Millicell chamber and coculture method were used to establish chemotactic migration model in vitro to observe the effect of genistein on directional chemotactic migration movement of SKOV3 cells.The protein expressions of cell surface adhesion molecule CD44v6,matrix metalloproteinases and tissue inhibitor of metalloproteinases MMP-9/TIMP-1 and MMP-2/TIMP-2 were determined by using immunocytochemical method and their mRNA levels were examined by in situ hybridization.Results Compared with control group,the directional chemotactic migration of SKOV3 were significantly decreased after treated with 20 ?mol/L and 40 ?mol/L genistein,reached to(46.9?5.8)% and(28.3?4.7)% respectively(P

OBJECTIVE To investigate the ?-lactamase genes and virulence gene in Escherichia coli isolated from the old patients.METHODS Twenty strains of E. coli were selected to test 15 kinds of ?-lactamase genes (TEM,SHV,CTX-M-1 group,CTX-M-2 group,CTX-M-9 group,OXA-1 group,OXA-2 group,OXA-10 group,PER,GES,VEB/CEF,CARB,DHA,ACT/MIR and LAT/CMY) and two virulence genes (CNF-1 and CNF-2).RESULTS Six ?-lactamase genes and one virulence gene have been found out from these 20 strains of E. coli. The results showed that there were 14,3,1,5,2,2 and 1 strain which carried TEM,SHV,CTX-M-1 group,OXA-1 group,DHA,ACT/MIR and CNF-1,respectively. These 20 E. coli strains contained at least 1 ?-lactamase gene and 7 E. coli strains were found containing more than 2 kinds of ?-lactamase at the same time.CONCLUSIONS The resistance of these 20 E. coli strains to ?-lactam antibiotics is closely relative to ?-lactamase.

After murine fetal liver cells (FLC) were transfected with granulocyte-macrophage colony-stimulating factor (GM-CSF) gene by recombinant adenovirus and intrasplenically transplanted into allogeneic mice, the effects of GM-CSF gene-transfected FLC on the recovery of immune response inhibited by chemotherapy were observed. The number of CD4 + cells and the ratio of CD4 + /CDS + cells from peripheral blood lymphocytes increased significantly. The cytotoxicity of the NK cells and the proliferation response of splenocytes to ConA, LPS elevated markedly, but the same results were not from bone marrow. These data demonstrated that intrasplenic transplantation of GM-CSF gene-transfected FLC could effectively accelerate the recovery of immune response after high-dose chemotherapy.

Objective: To study the effects of genistein on the expression of urokinase-type plasminogen activator (uPA) and the activity of protein tyrosine kinase (PTK) in MDA-MB-453 cells, and explore the molecular mechanism of anti-angiogenesis in HER-2/neu-overexpressing breast cancer by genistein. Methods:Western blot, immunoprecipitate, reverse transcription-polymerase chain reaction (RT-PCR) and kinase activity analysis technics were used to observe the expression of uPA and the protein phosphorylation of HER-2/neu receptor and the activity of protein tyrosine kinase (PTK) in MDA-MB-453 cells treated by genistein for 24, 48, 72 h. Results: The expression of uPA and the protein phosphorylation of HER-2/neu receptor and the activity of PTK were significantly decreased after treated with 5?10-5mol/L genistein, which had a time-dependence. Conclusion: Genistein could inhibit the activity of PTK and the protein phosphorylation of HER-2/neu receptor, and down-regulate the exprssion of uPA at transcription and translation levels in breast cancer cells. This might be a part of molecular mechanism of genistein anti-angiogenesis in HER-2/neu-overexpressing breast cancer.

Objective To establish the animal model of photochemical damage and investigate the protective effects and mechanism of taurine on the retina photochemical damage in rats. Methods Fifty rats were randomly divided into normal control group, light damage group and 4% taurine supplementation group. After 15 day cyclic light and 24-hour dark adaptation, the last two groups were exposed to (3000?200) lx transmitted by six cold white lights. After 24-hour exposure, the rats were stayed in darkness. The retinal morphology was detected through light and electron microscope and the retinal function was detected by Scot-ERG. The concentration of MDA and the activity level of SOD/GSH-px were measured. Results In light damage group, the a and b amplitude (Aa/Ab) were significantly decreased, but in taurine group, except the decreased Aa, others were of no significant changes. The retina inner and outer segments were swollen and in disorder after exposure, the outer nuclear layer got thinner than that of control. The mitochondria in light damage group was swollen, but in taurine group changes were less significant. After exposure, the concentration of MDA in retina was markedly increased in light damage group and the activity level of SOD/GSH-px were decreased, but in taurine group MDA slightly increased and SOD/GSH-px was up-regulated but of no significance. Conclusion Dietary supplementation with 4% taurine partially protected photoreceptor from degeneration, which might correlate with the antioxidation and inhibition of free radical character of taurine.

Objective To explore the inhibitory effect of genistein on oncogene HER-2/neu-overexpressing breast cancer xenograft tumors and its relationship with urokinase type plasminogen activator (uPA) expression. Methods HER-2/neu-overexpressing MCF-7 human breast cancer cells (MCF-7/HER-2) were generated by transfecting the HER-2/neu negative MCF-7 cells with HER-2/neu cDNA. MCF-7/HER-2 and MCF-7 xenograft models were established in BALB/c nude mice, and the nude mice with MCF-7/HER-2 xenograft were randomly divided into three groups: control group, genistein-treated group, and HER-2/neu antibody-treated group. The growth ability of xenograft tumors was analyzed by immunohistochemical staining with Ki-67 antibody, and uPA expression of xenograft tumors was analyzed by Western blotting. Results The growth ability and uPA expression were significantly higher in MCF-7/HER-2 xenograft tumors than those in MCF-7 xenograft tumors. MCF-7/HER-2 xenograft tumors treated by genistein or HER-2/neu antibody showed lower growth ability and uPA expression as compared with MCF-7/HER-2 xenograft tumors. Conclusion Genistein can inhibit the growth ability of HER-2/neu-overexpressing breast cancer xenograft tumors, which is associated with the uPA expression.

Objective: To observe the effects of taurine (Tau) on photoreceptor apoptosis and investigate the mechanism. Method: Seventy rats were randomly divided into control group (Cont) and 4% taurine supplementation group (Tau). The subjects were exposed to the cool white light (3000?200 lx)for 0, 1, 3, 6, 9, 12 or 24 h . The apoptotic index (AI) of photoreceptor was evaluated by TUNEL method. Meanwhile, levels of p65 in nuclear and caspase-1 were determined by Western-blot analysis and I?Ba mRNA was detected by RT-PCR . Results: After 9 h exposure, scattered TUNEL positive photoreceptors were found in Tau group, and each AI was lower than the corresponding control (P

Objective To investigate the Shenmai injection for the inhibition of hepatic and renal toxicity and leukocyte disorder during chemoradiotherapy in the women with advanced breast cancer. Methods 58 cases of female breast cancer patients with stage Ⅳ were selected and randomly divided into 2 groups, 29 cases of each group, and patients were treated with 5-hydroxytryptamine (5-HT3) receptor antagonists and white blood cell growth hormone and other conventional therapy, the control group received gemcitabine plus cisplatin chemotherapy, 28d for 1 cycles, the treatment group received more with Shenmai injection, interval was 15d, 2 groups were treated for 3 cycles. Levels of peripheral blood T lymphocyte subsets, cytokine levels and liver and kidney function, quality of life and clinical efficacy were compared. Results Compared with before treatment, levels of CD3+, CD4+ and CD4+/CD8+ in control group decreased (P<0.05), levels of CD3+, CD4+ and CD4+/CD8+ in treatment group increased (P<0.05), levels of CD8+ decreased(P<0.05), levels of IFN-γ, IL-2 and TNF-α increased(P<0.05), levels of IL-6 decreased(P<0.05), scores of KPS increased(P<0.05), scores of FACT-B decreased(P<0.05), levels of ALT, AST, BUN increased(P<0.05), and levels of CCr, WBC counts decreased(P<0.05), and compared with the control group, levels of CD3+ , CD4+ and CD4+/CD8+ in the treatment group were higher(P<0.05), levels of CD8+ were lower(P<0.05), levels of IFN-γ, IL-2 and TNF-α were higher(P<0.05), levels of IL-6 were lower(P<0.05), and the total efficiency was higher(P<0.05), levels of ALT, AST, BUN were lower (P<0.05), and levels of CCr, WBC counts were higher (P<0.05). After treatment, the efficacy of treatment group was higher than that of control group(Z=-2.142,P=0.032<0.05). Conclusion Shenmai injection can improve the efficacy of radiotherapy and chemotherapy in patients with advanced breast cancer, and it can effectively inhibit the liver and kidney damage and leukocyte disorder.

Objective To investigate the mechanisms of genistein in the growth inhibition in the tumor angiogenesis. Methods The effects of genistein and vascular endothelial growth factor receptor (VEGFR) on the proliferation of ECV304 cells were observed by cell growth curves and flow cytometry. The level of the phosphorylation of VEGFR and the activity of protein tyrosine kinase (PTK) in ECV304 cells were detected by immunoprecipitation and kinase activity analysis. Results Vascular endothelial growth factor (VEGF) alone could facilitate the proliferation of ECV304 cells, up regulate the phosphorylation and PTK activity of VEGFR, but genistein alone could inhibit the growth of ECV304 cells, stop the cell cycle mainly at the phase of G 2/M, induce apoptosis, and down regulate the phosphorylation and PTK activity of VEGFR ( P