8 research outputs found
Top: western blotting of the levels of pro-caspase-9 and caspase-9; centre: pro-caspase-8 and caspase-8; and bottom: pro-caspase-3 and caspase-3 proteins.
<p>Caco-2 cells were treated with MA at IC<sub>50</sub> and IC<sub>80</sub> concentrations for 4 h. The levels of protein expression are expressed as arbitrary intensity units of each band compared to arbitrary intensity units of actin. The values represent means ± S.D. of at least three independent experiments performed in triplicate. Key: <i>(*) p<0</i>.<i>05</i>, <i>(**) p<0</i>.<i>01</i> and <i>(***) p<0</i>.<i>001</i>, with respect to the untreated control cells.</p
Western blotting to determine Bid and t-Bid levels in Caco-2 cells (Top) and HT29 cells (Bottom).
<p>Caco-2 and HT29 cells were treated with MA at IC<sub>50</sub> and IC<sub>80</sub> concentrations for 4 h. The levels of protein expression are expressed as arbitrary intensity units of each band compared to arbitrary intensity units of actin. MA produced clear effects on this protein in Caco-2 cells. However, this effect was not observable in HT29 cells. The values represent means ± SD. of at least three independent experiments performed in triplicate. Key: <i>(*) p<0</i>.<i>05</i> and <i>(**) p<0</i>.<i>01</i>, with respect to the untreated cells.</p
Schematic representation of the different mechanisms proposed for the induction of apoptosis by MA in colon-cancer Caco-2 cells (right) and HT29 cells (left).
<p>MA is able to activate both intrinsic and extrinsic apoptotic mechanisms according to the type of cell involved. <i>Abbreviations</i>: Cps, caspase; cit c, cytochrome-c.</p
List of metabolites identified for <sup>1</sup>H NMR data by Chenomx database in Apc<sup>Min/+</sup> mice serum.
<p>↑/↓ Higher/Lower in MA-fed group when compared with the control diet group.</p>‡<p>Ratio between the area under the curve (AUC) in MA and the AUC in controls for the corresponding metabolite.</p>$<p>p-value relative to difference between MA and control.</p
MA feeding inhibits intestinal polyposis in APC<sup>Min/+</sup> mice.
<p>A) Total number of polyps/mouse in the small intestine of Apc<sup>Min/+</sup> mice. B) Number of polyps/mouse in proximal, medial and distal sections. C) Number of polyps/mouse shown by polyp size distribution (<1 mm diameter polyps, 1–2 mm and >2 mm). Data represented as mean ± SEM (* *, p<0.01).</p
Pathways modified in the colon mucosa of Apc<sup>Min/+</sup> mice by MA treatment as found in Metacore.
<p>More significantly modulated pathways in Metacore using genes with FC>1.5 and adjusted p-value<0.01. ↑/↓, activation/inhibition of the biological process by MA;</p>$<p>p-value that corresponds to the GeneGO Map/Pathway.</p>‡<p>Ratio between the number of significantly modulated genes by MA and the total number of genes per GenenGO Map/Pathway in Metacore.</p
Body weight and diet consumption monitoring.
<p>A) Effects of MA treatment on body weight. B) Effects of MA feeding in food intake. Data represented as mean ± SEM (* *, p<0.01).</p
Validation of genes that were differentially expressed in the colon mucosa of Apc<sup>Min/+</sup> mice after MA treatment by RT-PCR.
<p>Mean ± SD are shown. *, p<0.05; * *, **p<0.01, versus the untreated condition. n = 8/group.</p