No abstract

In this study, we investigated anti‐glycation effects on gold nanoparticles. It has been known that protein aggregation leads to make advanced glycation end‐products (AGEs) synthesis, and AGEs can be a diabetes‐ and aging‐causing factor. The aqueous solution (500mL) of 1–2 mM HAuCl4 was brought to a reflux and stirred, and then 50mL of 38.8mM trisodium citrate solution was added quickly, which resulted in a solution color change from pale yellow to deep red. We employed SEM to measure their sizes of gold nanoparticles, and glycation reaction with BSA and glycoaldehyde. Aminoguanidine, a well‐known anti‐glycation compound, is used as a positive control. The reaction mixture contained 6.02*10^17 atoms/mL and 1.204*10^18 atoms/mL of Au. We found that 13 nm‐nano sized gold particles showed anti‐glycation effects dose‐dependently suggesting a possible role of these particles against protein glycation reaction.

Maillard reaction is a nonenzymatic reaction between an amino acid and a reducing sugar that usually occurs upon heating. This reaction occurs routinely in cooking and its products are considered as safe materials. In this study, various MRPs samples were prepared from three different amino acids (lysine, arginine and glycine) and sugars (glucose, fructose and galactose) for 1 h heating at 121¡É. Treatments with the MRPs samples on RAW264.7 cells stimulated with lipopolysaccharide (LPS) decrease nitric oxide (NO) expression compared to control. Moreover, a MRPs sample derived from lysine and galactose most significantly inhibited NO expression. We also evaluated antiinflammatory effect of MRPs with a co‐culture system consisting of Caco‐2 intestinal epithelial cell line (apical side) and RAW264.7 macrophage cell line (basolateral side) to investigate the gut inflammation reaction. In this system, RAW264.7 cells stimulated with LPS decreased transepithelial electrical resistance (TEER), which is a marker of the integrity of cells, and increased TNF‐α productions and gene expressions of IL‐8 and IL‐1¥â in Caco‐2 cells. In this system, ultrafiltration fractions with high molecular weight suppressed IL‐8 gene expression as well as reduction of TNF‐α production from RAW264.7 cells stimulated with LPS.

No abstract

Atherosclerosis is one of the consequence of long‐term diabetic complications due to the accumulation of lipids and fibrosis in the artery wall. Advanced glycation endproducts (AGEs) may play an important role in the pathogenesis of diabetic complications. Atherosclerosis initiates adhesion of monocytes which induced by AGEs to the endothelium and transmigration across tight‐juction of endothelial cells (EC) into intima. Monocytes differentiated into macrophages which uptook lipoproteins and became foam cells. Smooth muscle cells (SMC) were then migrated from media to surface and secreted various fibrous elements. The aim of this study is to confirm the proliferation of SMC by AGE in a co‐culture system in which monocyte, EC and SMC were employed. THP‐1, human acute monocytic leukemia cells and HUVEC, human umbilical vein endothelial cells were cultured for 48 hours on the 2% gelatin coated upper chamber and HA‐VSMC, human artery vascular smooth muscle cells in the lower chamber. In a group treated with AGEs, SMC were co‐cultured with HUVEC and THP‐1 with 100 μg/mL of AGEs for 48 hours. Proliferation of SMC was measured by MTT assay. We observed proliferation of SMC by AGEs that using our co‐culture system. Moreover, AGEs treated SMC also induced several fibroblast markers on mRNA levels including fibronectin, collagen type 3 by this co‐culture system.