Prenylated polyphenols from <i>Clusiaceae</i> and <i>Calophyllaceae</i> as regulators of inflammation and immunity: Overview and hypothesis.

<p>(1) NPs efficiently inhibit the induction of VCAM-1, an adhesion molecule involved in the firm adhesion of leukocytes on inflamed endothelium and a prerequisite step for leukocyte activation (2) and extravasation in the tissues. (3) NPs strongly impair the expression of MHC molecules expressed on endothelium and involved in innate and adaptive immunity via the activation of NK and CD4T and CD8T cells, respectively.</p

Effect of NPs 1–6 and 8–11 on endothelial cell viability.

<p>Cell viability was assessed on confluent EC monolayers using MTT assay. Cells were incubated with NPs (10 μM) for 48h before analysis. Diluted DMSO (1/1000 –dark dashed line) was used as control for diluent (Dil), as well as a non-treated (NT) control—grey dashed line—and the cytotoxicity positive control glyoxal (Gly) at 4 mM. The cytotoxic activity of the immunosuppressive drug zoledronic acid (ZA, 10 μM) was also assessed. Statistical analysis of values (O.D.) obtained for treated versus non-treated cells were performed using non-parametric ANOVA test.</p

Effect of compounds 1–6 and 8–11 on TNF-induced expression of inflammatory molecules in ECs.

<p><b>(A) Basal <i>versus</i> TNF-induced expression of VCAM-1, ICAM-1 and E-selectin after 6h of incubation.</b> Data shown are representative histograms from fluorescence-activated cell sorting (Facs) analysis showing constitutive <i>versus</i> induced expression of inflammatory molecules (VCAM-1, ICAM-1, E-selectin) at the cell surface of ECs. Histograms show the intensity of fluorescence (log, x-axis) versus cell number (y-axis) for untreated (purple line) and cytokine-treated (green line) ECs analyzed by flow cytometry. Immunostaining using an irrelevant isotype-matched IgG (dark line) was used as a negative control. (<b>B</b>) <b>Inhibitory effects of NPs.</b> Expression of VCAM-1, ICAM-1 and E-selectin was measured by Facs. Each bar represents geometric mean ± SD of fluorescence intensity calculated from three to five independent experiments. Statistical analysis was performed using Kruskal-Wallis test with Dunn’s post-test; *<i>p</i> < 0.05, **<i>p</i> < 0.01, ***<i>p</i> < 0.001 compared with TNF control group. PDTC (200 μM) was used as a positive control for inhibition.</p

Basal <i>versus</i> IFNγ-modulated expression of MHC class I, MHC class II, HLA-E and MICA on EC cultures.

<p>ECs were treated with or without IFNγ for 48h before analysis. Data shown are representative histograms from Facs analysis showing constitutive <i>versus</i> IFNγ-regulated expression of inflammatory molecules (MHC class I, MHC class II, HLA-E and MICA) at the EC surface. Histograms show the intensity of fluorescence (log, x-axis) <i>versus</i> cell number (y-axis) for untreated (purple line) and cytokine-treated (green line) ECs analyzed by flow cytometry. Immunostaining using an irrelevant isotype-matched IgG (dark line) was used as a negative control.</p

Chemical Composition, Antioxidant and Anti-AGEs Activities of a French Poplar Type Propolis

Accumulation in tissues and serum of advanced glycation end-products (AGEs) plays an important role in pathologies such as Alzheimer’s disease or, in the event of complications of diabetes, atherosclerosis or renal failure. Therefore, there is a potential therapeutic interest in compounds able to lower intra and extracellular levels of AGEs. Among them, natural antioxidants (AO) with true anti-AGEs capabilities would represent good candidates for development. The purpose of this study was to evaluate the AO and anti-AGEs potential of a propolis batch and then to identify the main compounds responsible for these effects. In vivo, protein glycation and oxidative stress are closely related. Thus, AO and antiglycation activities were evaluated using both DPPH and ORAC assays, respectively, as well as a newly developed automated anti-AGEs test. Several propolis extracts exhibited very good AO and anti-AGEs activities, and a bioguided fractionation allowed us to identify pinobanksin-3-acetate as the most active component