Abstract
Advanced glycation endproducts (AGEs) is implicated in the pathogenesis of diabetic complications. Inhibiting the formation of AGEs and interfering with AGEs-mediated inflammation are two practicable strategies for developing a dietary adjuvant against diabetic complications. This study evaluated the protective capacities against diabetic complications of several spices based on their inhibition of the formation of AGEs in an in vitro BSA/glucose system and on the AGEs-induced production of proinflammatory cytokine in RAW 264.7 macrophages. Among the tested spices, cinnamon exhibited most strongly inhibited both the formation of AGEs and the AGEs-induced production of nitric oxide, interleukin-6 and tumor necrosis factor-α. Additionally, correlative results revealed that the capacity of spices to inhibit the formation of AGEs is attributable to phenolic compounds and, in contrast, the capacity to inhibit AGEs-induced inflammation is attributable to condensed tannin. This investigation demonstrates the potential of cinnamon to serve as a dietary adjuvant against diabetic complications.
Highlights
During recent decades, growing evidence has shown that advanced glycation end-products (AGEs) participate importantly the pathogenesis of diabetic complications [1,2]
This study evaluated the protective capacities against diabetic complications of several spices based on their inhibition of the formation of Advanced glycation endproducts (AGEs) in an in vitro bovine serum albumin (BSA)/glucose system and on the AGEs-induced production of proinflammatory cytokine in RAW 264.7 macrophages
Correlative results revealed that the capacity of spices to inhibit the formation of AGEs is attributable to phenolic compounds and, in contrast, the capacity to inhibit AGEs-induced inflammation is attributable to condensed tannin
Summary
During recent decades, growing evidence has shown that advanced glycation end-products (AGEs) participate importantly the pathogenesis of diabetic complications [1,2]. The engagement of AGEs with RAGE triggers NADPH-oxidase, increasing intracellular oxidative stress, evoke signaling pathways such as protein kinase C, mitogen-activated protein kinase and the extracellular signal regulated kinase; activate transcription factor NF-κB and AP-1, and subsequently induce thrombogenic, fibrogenic, adhesive, chemoattractive and proinflammatory gene expression [3]. This AGEs-induced oxidative stress, fibrosis and inflammation accelerate the progress of diabetic vascular complications [4]. Agents that block the formation of AGEs, including aminoguanidine, thiamine and pyridoxine, and those that suppress AGEs-induced inflammation such as secreted form of RAGE (sRAGE), which blocks RAGE, have yielded promising results in animal models [5]
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