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|標題:||Naturally occurring flavonoids attenuate high glucose-induced expression of proinflammatory cytolkines in human monocytic THP-1 cells||作者:||Wu, C.H.
|關鍵字:||Advanced glycation endproducts;CM L;Flavonoids;Glucose;Oxidative;stress;glycation end-products;factor-kappa-b;oxidative stress;cyclooxygenase-2 expression;diabetic complications;molecular-mechanisms;mononuclear-cells;cellular receptor;bcl-2;expression;rage||Project:||Molecular Nutrition & Food Research||期刊/報告no：:||Molecular Nutrition & Food Research, Volume 53, Issue 8, Page(s) 984-995.||摘要:||
Activation of circulating monocytes by hyperglycemia is bound to play a role in inflammatory and atherosclerosis. In this study, we examined whether flavonoids (catechin, EGCG, luteolin, quercetin, rutin) - phytochemicals that may possible belong to a new class of advanced glycation end products (AGEs) inhibitors - can attenuate high glucose (15 mmol/L, HG)-induced inflammation in human monocytes. Our results show that all flavonoids significantly inhibited HG-induced expression of proinflammatory genes and proteins, including TNF-alpha, interleukin-1 beta (IL-1 beta), and cyclooxygenase (COX)-2, at a concentration of 20 mu M. Flavonoids also prevented oxidative stress in activated monocytes, as demonstrated by their inhibitory effects on intracellular reactive oxygen species (ROS) and N(epsilon)-(carboxymethyl)lysine formation caused by HG. These inhibitory effects may involve inhibition of nuclear factor-kappa B activation and may be supported by downregulation of the following: i) PKC-dependent NADPH oxidase pathway; ii) phosphorylation of p38 mitogen-activated protein kinase and extracellular signal-regulated protein kinase, and iii) mRNA expression of receptor of AGEs. In addition, we found for the first time that lower levels of Bcl-2 protein under HG conditions could be countered by the action of flavonoids. Our data suggest that, along with their antioxidant activities, flavonoids possess anti-inflammatory properties and might therefore have additional protective effects against glycotoxin-related inflammation.
|Appears in Collections:||食品暨應用生物科技學系|
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