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Objective:Comprehensive assessment of the chemical composition of sage leaves (Salvia officinalisL.)in order to highlight constituents relevant to the antioxidant, antimicrobial and anticancer potentials, in addition to determining safe dose to facilitate its application in functional foodsand dairy products. Methods:High-Performance Liquid Chromatography (HPLC) was employed to determine constituents such as amino acids, fatty acids and phenolic compounds content. Antioxidant activity was characterized using, ?-diphenyl-?-picrylhydrazyl (DPPH) and reducing power methods. The antimicrobial potentials were examinedagainst nine pathogenic strains. MDA-MB-231 cell line was used to assess anticancer activity. Results:Sage was found to be a good source of calcium, iron andzinc (894.3, 84and 5.5 mg/100g respectively) and vitamins B6 and B12(1.5 and 0.3 mg/100g respectively). PerformedHPLC analysis indicated the rich content of essential amino acids, lysine, phenylalanine andleucine (10.4, 0.7 and 0.45 g/100g),unsaturated fatty acids, Omega 3, 6 and 9(6.46, 4.40 and 3.13g/100g) and phenolic compounds, quercetin and cinnamic (604.8 and 390.4 ?g/mL),which interpreted its high antioxidant powers. Sage revealed antioxidantpotentials with IC50and EC50 reached(27.5 and 239.5 mg/mL respectively), and antimicrobial effect against the examined pathogenic strains with MICs reached 6.25 mm against Staph.aureus, E. coliand Candida albicans, not to mention its anticancer effect as an extra pharmacological feature, when sage performed an anti-proliferative activity with IC50of 300 ?g/mL, against MDA-MB-231 cell line.Conclusion:Obtained results emphasis the sage leaves content of variable nutrients and active compounds that reflected on its vast nutritional and pharmacological potentials such as; antioxidant, antimicrobial and cytotoxic effect against breast MDA-MB-231 cell line, that could nominate it as applicable food bio-preservativein functional foods and dairy products
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Objective@#To investigate the properties of radiation-induced changes of cell cycle and apoptosis in breast cancer cell lines MDA-MB-231 and MCF-7, and to further explore its relationship with radiosensitivity.@*Methods@#The two cell lines MCF-7 and MDA-MB-231 were irradiated with 6 MV X-rays. The cell survival curves were fitted by clonogenic formation assay, then according to the radiosensitivity parameters average lethal dose (D0), quasi-threshold dose (Dq) and survival fraction after 2 Gy irradiation (SF2), the radiosensitivity of the two cell lines was compared. The apoptosis rate and cell cycle distribution of the two cell lines were detected by Hoechst 33342 and PI staining.@*Results@#The survival curve of MDA-MB-231 cell line shifted to the right compared with that of MCF-7 cell line. The values of D0, Dq and SF2 of MDA-MB-231 cell line were higher than those of MCF-7 cell line (1.603±0.023 vs. 1.233±0.027, 1.76±0.04 vs. 1.03±0.10, 0.639 3±0.008 2 vs. 0.398 1±0.018 5, t values were -17.981, -11.745, -20.596, P values were 0.000, 0.003, 0.000). The apoptosis rate of MCF-7 cell line was significantly higher than that of MDA-MB-231 cell line at the doses of 2, 4, 8 Gy irradiated 24 h and at the 12, 48 h after 6 Gy X-irradiation (t values were 4.441, 7.299, 10.499, 6.375, 7.743, P values were 0.011, 0.002, 0.000, 0.003, 0.001). Compared with the non-irradiated group, G2 phase arrest appeared in both cell lines after irradiation. The percentage of the G2/M phase in MDA-MB-231 cell line increased as the time or dosage accumulated. Furthmore, the percentage didn't go down even after 48 hours later. However, the blockage began to gradually release in MCF-7 cell line at the dose of 8 Gy irradiated 24 h and the 48 h after 6 Gy X-irradiation. Followed with that, it turned out the percentage of the G0/G1 phase increased [(65.80±0.56)%, (62.53±0.67)%].@*Conclusions@#6 MV X-irradiation with the doses of 2-8 Gy can induce the cell cycle arrest at G1 and G2 phase in MCF-7 cell line, G2 phase in MDA-MB-231 cell line. Thus more apoptosis appears in MCF-7 cell line, which may cause the difference in radiosensitivity between the two cell lines.
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OBJECTIVE: To investigate the potential anticancer effect of combretastatin A4 liposomes (SSL-CA4) in destruction of vascular mimicry (VM) in MDA-MB-231 breast cancer cells in vitro. METHODS: The in vitro inhibitory effect and blocking woundhealing effect of SSL-CA4 were investigated. The VM destruction of SSL-CA4 was evaluated in three dimensional matrigel culture model in MDA-MB-231 cells. The in vitro inhibitory test showed that the maxium inhibition ratio of SSL-CA4 on MDA-MB-231 cells was close to 50%. SSL-CA4 blocked the wound-healing of MDA-MB-231 cells, which was similar to free CA4. RESULTS: SSL-CA4 could inhibit the formation of VM in vitro via inhibition on the VM channel indicators including hypoxia-inducible factor (HIF-α), vascular endothelial- cadherin (VE-Cad), and matrix metallopeptidases (MMP-2). The inhibition on indicators of SSL-CA4 was significantly higher than CA4 treatment groups (P <0.05). CONCLUSION: SSL-CA4 has significant anticancer activity via inhibition of VM in MDA-MB-231 cell line.
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Objective To observe the migration and inhibition mechanism of MicroRNA218-Robo1 pathway for breast cancer.Methods A total of 40 BALB/c-nu/nu female mice were randomly divided into four groups.Each group was transfected over-expression MicroRNA218 MDA-MB-231 breast cancer cells, co-over-expression MicroRNA218 and Robo1 MDA-MB-231 breast cancer cells, knock-down Robo1 MDA-MB-231 breast cancer cells and the control MDA-MB-231 breast cancer cells.The tumor volume was examined every two weeks.Results Tumor volume of MicroRNA218 group was obviously less than control group, tumor volume of Robo1 knock out group was obviously less than common MicroRNA218 high expression and Robo1 group, the difference was statistically significant;MicroRNA218 and Robol knockout group than the control group, the increase in breast cancer cells apoptosis, cell proliferation and angiogenesis is restrained.Conclusions MicroRNA218 inhibited the migration of breast cancer by down-regulating the expression of Robo1.
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Objective To investigate four methods for establishing animal models of human breast cancer bone metastasis. Methods Thirty-two female nude mice aged 4-6 weeks were divided randomly into four groups (n=8 in each group). 5×105 MDA-MB-231 cells were injected into the body via the left second mammary fat pads (group A), the tail veins (group B), the left heart ventricles (group C) and the left tibia marrow cavities (group D), respectively. Tumor formations in situ were recorded in group A. Deaths after the injection were recorded. The surviving nude mice 49 days after the injection were subjected to pathological examination to determine bone metastasis. Results The rate of tumor formation in situ of group A was87.5 %(7/8). One mouse in group C died after the injection of MDA-MB-231 cells. The bone metastasis rate in groups A, B, C and D was zero (0/8), 12.5 % (1/8), 71.4 % (5/7) and 100 % (8/8), respectively. There was statistically significant difference in the bone metastasis rate between group A and group C, group A and group D, group B and group C; and group B and group D. Conclusion Injections of tumor cells via the breast fat pads and tail veins were not suitablemethods to establish animal models of human breast cancer bone metastasis. The bone metastasis model could be established efficiently by injecting tumor cells into the left heart ventricles or the bone marrow cavity of nude mice.
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Objective:To investigate the influence of histone deacetylase inhibitor(Trichostatin A)to multiplication,invasion, cell cycle of breast cancer MDA-MB-231 cell line.Methods:After 6-48hours treatment with the concentration(100～400nmol/L)of Trichostatin,the growth activity of MDA-MB-231 cell line was detected by MTT.The expression of ER?,MMP-9 mRNA was detected by RT-PCR with different concentration(100～400nmal/L TSA)during 24 hours to MDA-MB-231 cell line.The expression of ER?,MMP-9 protein was examined by immunohistochemistry with different concentration(100～400nmol/L TSA)during 24 hours treatment to MDA-MB-231 cell line.With cell invasion experiment to detect the change of invasive power by using different concentration(100～400nmol/L TSA)during 24 hours to MDA-MB-231 cell line.Results: Trichostatin can inhibit the growth of MDA-MB-231 cell line,which was time and dose dependent.Trichostatin can delay the cell cycle G_2/M stage,stop the cell stage in G_2 stage.Trichostatin can up-regulate the expression of ER?mRNA, down-regulate the expression of MMP-9 mRNA in cells.The invasion experiment indicate that Trichostatin can conspicuous inhibit the invasion of MDA-MB-231 cell line.Conclusions:Trichostatin can inhibit the accrementition,invasion and metastasis of MDA-MB-231 cell line evidently,and one of the mechanism may be the up-regulation of ER?and the down-regulation of MMP-9.