13 research outputs found

    HPRP-A2-induced BGC-823 and SGC-7901 cell death.

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    <p>The cells were treated with different concentrations of HPRP-A2 for 1 hour. Cell viability was determined using the MTT method. Results are expressed as percentage of the control ± SD of three independent experiments. Statistical analysis compared the HPRP-A2 treatment group with the control groups (*P < 0.005; **P <0.001).</p

    HPRP-A2-induced mitochondrial membrane potential.

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    <p>(A) BGC-823 cells were treated for 1 h and the generation of reactive oxygen species (ROS) was analyzed by FACS to quantitatively compare the fluorescence intensity (in Geomean) at various concentrations. (B) After 1 h treatment, the ratio of FL2-H/FL1-H decreased, indicating a reduction of MMP. (C) BGC-823 cells were treated with HPRP-A2 (10 and 15 μM) for 24 h and then levels of caspase activities were measured. Data are expressed as mean ± SD of three independent experiments. Statistical analysis compared the HPRP-A2 treatment group with the control groups (*P < 0.005; **P <0.001).</p

    Membrane permeability changes of BGC-823 cells by monitoring PI and LDH.

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    <p>The cells were incubated with increasing peptide concentrations for 1 h at 37 oC. (A) Quantitative comparisons of fluorescence intensity (in Geomean) at various concentrations were analyzed by flow cytometry. (B) LDH in the supernatant was measured with a microplate reader at 450 nm. Cells without treatment or lysed with triton X-100 was used as negative and positive controls, respectively. LDH activity was calculated as the percentage of experimental group and positive control, after subtraction of negative control respectively (*P<0.005). Data are the mean ± SD of three independent experiments.</p

    Cell viability and combination index of BGC-823 and SGC-7901 treated with a drug combination.

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    <p>Panel (A, B and C) represents growth inhibition in BGC-823 and SGC-7901 cells with a combination of HPRP-A2 (6 μM) and DOX (1.6 μg/ml) after incubation for 4, 24 and 48 hours, respectively. Results are expressed as the percentage of the control ± SD of three independent experiments. Panel D shows combination index (Q) of the combination treatment of HPRP-A2 and DOX, where Q<0.85, Q>1.15 and 0.85</p

    Hemolytic activity of HPRP-A2 against hRBCs.

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    <p>Data points present mean ± S.D. of three independent experiments. PBS and dH2O were used as negative and positive controls, respectively. Statistical analysis compared the HPRP-A2 treatment group with the positive control groups (*P < 0.005; **P <0.001).</p

    HPRP-A2 triggered cell cycle arrest.

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    <p>Cell-cycle distributions after treatment with 5, 10 and 15 μΜ HPRP-A2 for 24 h separately were detected by flow cytometry. Cell-cycle distributions were assessed by PI staining. The results were showed from one of three experiments with similar results.</p

    Cellular uptake and interaction between peptides and cell membranes.

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    <p>(<b>A</b>) The fluorescence time profiles of interaction between peptides and membranes. HeLa cells were incubated with different concentrations of FITC-labeled HPRP-A1 and HPRP-A1-TAT at concentrations of 2, 4, and 8 μM. Images (400× magnification) were captured by laser scanning confocal microscopy every 30 s from 0 to 180 s. Green, FITC peptides; blue, 4,6-diamidino-2-phenylindile-stained nuclei. (<b>B</b>) LDH leakage assay. HeLa cells were incubated with HPRP-A1 and HPRP-A1-TAT at 2, 4, and 8 μM for 1 h and LDH assayed. (<b>C</b>) Cellular uptake of peptides, measured by flow cytometry. After incubation for 1 h at 4°C, HeLa cells were incubated with FITC-HPRP-A1 or FITC-HPRP-A1-TAT peptides for 1 h. The cells were those cultured and treated with peptides at 37°C were used as controls. Data are presented as the mean ± SD of three independent experiments. LDH, lactate dehydrogenase.</p

    Circular dichroism spectra of peptides.

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    <p>(<b>A</b>) In benign medium (50 mM KH<sub>2</sub>PO<sub>4</sub>/K<sub>2</sub>HPO<sub>4</sub> containing 100 mM KCl, pH 7.4) at 25°C and (<b>B</b>) in the presence of 50% TFE at 25°C. The symbols used are as follows: ■, HPRP-A1 peptide; ▲, HPRP-A1-TAT peptide.</p

    Anticancer (IC<sub>50</sub>) and hemolytic activities (MHC) of peptides against cancer cells and human red blood cells.

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    <p><sup>a</sup>Anticancer activity (IC<sub>50</sub>) represents the concentration of peptides at which cell viability was inhibited by 50% in comparison with the untreated cells. The MTT assay was repeated in triplicate, and IC<sub>50</sub> value was determined by averaging three repeated experiments.</p><p><sup>b</sup>GM of the anticancer activity (IC<sub>50</sub>) for the four cancer cell lines.</p><p><sup>c</sup>Hemolytic activity (MHC) was determined using human red blood cells after incubation with peptides for 1 h. If no hemolytic activity was observed at 500 μM, a value of 1000 μM was used for calculating the therapeutic index.</p><p><sup>d</sup>Therapeutic index = MHC/IC<sub>50</sub>. Larger values indicate greater anticancer specificity.</p><p>GM, geometric mean; MHC, minimal hemolytic concentration.</p><p>Anticancer (IC<sub>50</sub>) and hemolytic activities (MHC) of peptides against cancer cells and human red blood cells.</p
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