ABSTRACT
The aim of the present work was to modify the exuded gum of Sterculia striata tree by an amination reaction. The viscosity and zero potential of the chicha gum varied as a function of pH. The modification was confirmed by X-ray diffraction (XRD), infrared spectroscopy (FTIR), size exclusion chromatography (SEC), zeta potential, thermogravimetric analysis (TG), and differential scanning calorimetry (DSC). Furthermore, the chemical modification changed the molar mass and surface charge of the chicha gum. In addition, the gums were used in tests for ex vivo mucoadhesion strength, antibacterial activity against the standard strain of Staphylococcus aureus (ATCC 25923), inhibitory activity of α-glucosidase, antioxidant capacity, and viability of Caco-2 cells. Through these tests, it was found that amination caused an increase in the mucoadhesive and inhibitory activity of chicha gum against the bacterium Staphylococcus aureus. In addition, the gums (pure and modified) showed antioxidant capacity and an inhibitory effect against the α-glucosidase enzyme and did not show cytotoxic potential.
Subject(s)
Antioxidants , alpha-Glucosidases , Humans , Antioxidants/pharmacology , Caco-2 Cells , Anti-Bacterial Agents/pharmacology , Anti-Bacterial Agents/chemistry , X-Ray Diffraction , Plant Gums/pharmacology , Plant Gums/chemistry , Spectroscopy, Fourier Transform InfraredABSTRACT
BACKGROUND: Because oestrogen receptor α (ERα) regulates E2F1 expression to mediate tamoxifen resistance in ERα-positive breast cancer cells, we aimed to define the possible roles of ERα and E2F1 in promoting the resistance of ERα-negative breast cancer cells to 4-hydroxy-tamoxifen (4OHT). METHODS: This study utilised conventional techniques to demonstrate the effects of 4OHT on the expression of ERα and E2F1 and also examined the individual and combined effects of 4OHT with dipyridamole (DIPY) and 3-O-(3,4,5-trimethoxybenzoyl)-(-)-catechin (TMCG) on the oestrogen-negative MDA-MB-231 breast cancer cell line using viability assays, Hoechst staining, MALDI-TOF mass spectroscopy, and confocal microscopy. RESULTS: Despite the ERα-negative status of the MDA-MB-231 cells, we observed that 4OHT efficiently up-regulated ERα in these cells and that this upregulation promoted E2F1-mediated cell growth. Because E2F1 plays a dual role in cell growth/apoptosis, we designed a therapy incorporating TMCG/DIPY to take advantage of the elevated E2F1 expression in these 4OHT-treated cells. 4OHT enhances the toxicity of TMCG/DIPY in these ERα-negative breast cancer cells. CONCLUSIONS: Because TMCG/DIPY treatment modulates the methylation status/stability of E2F1, the results demonstrate that therapies targeting the epigenetic machinery of cancer cells in the presence of overexpressed E2F1 may result in efficient E2F1-mediated cell death.
