I thought this was interesting. I'm taking quercetin as a resveratrol synergist, but it also has some nice effects in it's own right. Luteolin seems interesting too, but it is way too expensive.
http://www.ncbi.nlm....l=pubmed_docsum
Flavonoids inhibit the formation of the cross-linking AGE pentosidine in collagen incubated with glucose, according to their structure.
* Urios P,
* Grigorova-Borsos AM,
* Sternberg M.
Equipe de recherche "Proteines modifiees, proteases et physiopathologie de l'endothelium vasculaire", Dept. de Biochimie, Faculte de Medecine & Laboratoire de Pharmacologie, Faculte de Pharmacie, Universite Rene Descartes, Paris, France.
BACKGROUND: Glycoxidation of collagens contributes to development of vascular complications in diabetes. AIM OF THE STUDY: Since flavonoids are potent antioxidants present in vegetal foods, it was interesting to examine their effect on the formation of a cross-linking advanced glycation endproduct, pentosidine, in collagens. METHODS: Collagen was incubated with glucose (250 mM), in the presence of different flavonoids. Pentosidine was measured by HPLC, hydroxyproline colorimetrically. RESULTS: Monomeric flavonoids (25 and 250 microM) markedly reduced pentosidine/hydroxyproline values in a concentration- and structure-dependent manner. In decreasing order of their specific inhibitory activity, they rank as follows: myricetin >/= quercetin > rutin > (+)catechin > kaempferol. Thus 3'-OH or 4-oxo + Delta(2-3) increase the inhibitory activity; conjugation by Rha-Glc on 3-OH decreases it. Procyanidin oligomers from grape seed were more active than pine bark procyanidin oligomers: this may be related to the galloyl residues present in grape seed oligomers only. Procyanidin oligomers are known to be cleaved into monomers in the gastric milieu and monomeric flavonoids to be absorbed and recovered at micromolar concentrations (with a long plasmatic half-life) in extracellular fluids, in contact with collagens. CONCLUSION: Flavonoids are very potent inhibitors of pentosidine formation in collagens. They are active at micromolar concentrations; these might be achieved in plasma of diabetic patients after oral intake of natural flavonoids.
PMID: 17356796 [PubMed - as supplied by publisher]
http://www.ncbi.nlm....l=pubmed_docsum
Inhibitory effect of naturally occurring flavonoids on the formation of advanced glycation endproducts.
* Wu CH,
* Yen GC.
Department of Food Science, National Chung Hsing University, 250 Kuokuang Road, Taichung 40227, Taiwan.
The objective of this study was to investigate the inhibitory effect of naturally occurring flavonoids on individual stage of protein glycation in vitro using the model systems of delta-Gluconolactone assay (early stage), BSA-methylglyoxal assay (middle stage), BSA-glucose assay, and G.K. peptide-ribose assay (last stage). In the early stage of protein glycation, luteolin, qucertin, and rutin exhibited significant inhibitory activity on HbA1C formation (p < 0.01), which were more effective than that of aminoguanidine (AG, 10 mM), a well-known inhibitor for advanced glycation endproducts (AGEs). For the middle stage, luteolin and rutin developed more significant inhibitory effect on methylglyoxal-medicated protein modification, and the IC50's were 66.1 and 71.8 microM, respectively. In the last stage of glycation, luteolin was found to be potent inhibitors of both the AGEs formation and the subsequent cross-linking of proteins. In addition, phenyl-tert-butyl-nitron served as a spin-trapping agent, and electron spin resonance (ESR) was used to explore the possible mechanism of the inhibitory effect of flavonoids on glycation. The results indicated that protein glycation was accompanied by oxidative reactions, as the ESR spectra showed a clear-cut radical signal. Statistical analysis showed that inhibitory capability of flavonoids against protein glycation was remarkably related to the scavenging free radicals derived from glycoxidation process (r = 0.79, p < 0.01). Consequently, the inhibitory mechanism of flavonoids against glycation was, at least partly, due to their antioxidant properties.
http://www.ncbi.nlm....l=pubmed_docsum
Effects of flavonoids on the expression of the pro-inflammatory response in human monocytes induced by ligation of the receptor for AGEs.
* Huang SM,
* Wu CH,
* Yen GC.
Department of Food Science and Biotechnology, National Chung Hsing University, Taichung, Taiwan.
Increasing evidence has shown advanced glycation end products (AGEs) receptor ligation (RAGE) to be an important part of complex interactions of the oxidative stress and pro-inflammatory responses. In this study, flavonoids were used to monitor the protective effects against the oxidative damage and inflammation mediated by AGEs in human monocytes. S100B (RAGE ligand) treatment in human THP-1 monocytic cells (THP-1) significantly increased gene expression of the pro-inflammatory cytokines TNF-alpha and IL-1beta; chemokines MCP-1 and IP-10; adhesion factors platelet endothelial cell adhesion molecule (PECAM-1) and beta2-integrin; and pro-inflammatory cyclooxygenase-2 (COX-2). S100B treatment with quercetin and catechin in THP-1 cells had inhibitory effects on the expression of pro-inflammatory genes and protein levels. Quercetin and catechin could regulate S100B-activated oxidant stress-sensitive pathways through blocking p47phox protein expression. Treatment with quercetin and catechin could eliminate reactive oxygen species (ROS) to reduce oxidative stress stimulated by S100B in THP-1 cells. Quercetin and catechin also showed different regulatory abilities on mitogen-activated protein kinase (MAPK) signaling pathways by inhibiting protein expression in S100B-stimulated inflammatory responses in THP-1 cells. This study suggests that quercetin and catechin may be of benefit for diabetic vascular complications due to its antioxidant abilities against AGE-mediated oxidative stress through oxidative stress-sensitive and oxidative stress-responsive signaling pathways, which lead to inflammation in human monocytes.
PMID: 17103373 [PubMed - indexed for MEDLINE]
