• Korean Journal of Oriental Medicine
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• v.9 no.1
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• pp.123-126
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• 2003

Advanced glycation end products(AGEs) are largly involved in the pathogenesis of diabetic complications. It is obvious that inhibition of AGEs formation is important in preventing the occurrence and progression of diabetic complications. Therefore, to seek possible AGEs inhibitors in herbal medicines, unprocessed - und processed Puerariae Radix were tested. The inhibitory effect on AGEs formation was slightly increased through processing. Unprocessed-, processed Puerariae Radix and puerarin showed potential inhibitory action than that of positive control, amino guanidine HCI.

• Korean Journal of Pharmacognosy
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• v.33 no.4 s.131
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• pp.308-311
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• 2002

Advanced glycation end products(AGEs) are largly involved in the pathogenesis of diabetic nephropathy. It is obvious that inhibition of AGEs formation is important in preventing the occurrence and progression of diabetic nephropathy. In diabetes, this reaction is greatly accerated and is important in the pathogenesis of diabetic complications, especially diabetic nephropathy. Therefore, to seek possible AGEs inhibitors in herbal medicines, unprocessed - and processed Magnolia Bark were examined in vitro as basic data for aniaml experiment. The content of magnolol in unprocessed Magnolia Bark was $0.796{\pm}0.072%$, and after processing was decreased to $0.586{\pm}0.101%(p<0.01)$. The content of AGEs was measured by their intrinsic fluorescence. The $IC_{50}({\mu}g/ml)$ values of aminoguanidine, unprocessed- and procesled Magnolia Bark are $38.845{\pm}8.36{\mu}g/ml$, $54.264{\pm}3.153{\mu}g/ml$ and $27.882{\pm}1.836{\mu}g/ml$, respectively. This result means that prcessed Magnolia Bark was more effective than aminoguanidine, as positive control.

• Journal of the Korean Society of Food Culture
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• v.39 no.6
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• pp.322-332
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• 2024

Advanced glycation end products (AGEs) trigger various metabolic diseases and accumulate in the organs during the onset of metabolic diseases. The AGE-receptor for AGE (RAGE) interactions are strongly associated with the onset of chronic renal disease and diabetic nephropathy. This study evaluated the effects of glyoxal-lysine dimer (GOLD) and methylglyoxal-lysine dimer (MOLD) accumulation on various mechanisms in SV40 MES 13 kidney cells, which are currently unclear. GOLD and MOLD showed different effects on oxidative stress, inflammation, mitochondrial dysfunction, autophagy, and apoptosis. GOLD did not induce cytotoxicity or interact with RAGE. By contrast, MOLD significantly reduced the cell viability and interacted with RAGE. This study tested whether the RAGE interaction could cause differences in the effects of GOLD and MOLD on the mechanisms studied. GOLD did not generate oxidative stress or interact with RAGE and did not show toxicity through other mechanisms. Nevertheless, MOLD caused oxidative stress, inflammation, mitochondrial dysfunction, and apoptosis, which are representative glucotoxicity mechanisms of AGE-RAGE interactions, and autophagy. Overall, these findings suggest that AGEs may show different toxicities in various organs. GOLD accumulation in the kidneys might not affect disease occurrence, but MOLD accumulation can promote disease.

• The Journal of Korean Medicine
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• v.37 no.2
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• pp.62-75
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• 2016

Objectives: This study examined whether Lycii Radicis Cortex has an inhibitory effect on inflammatory response through an oxidative stress and advanced glycation endproducts (AGEs)-mediated pathway in streptozotocin (STZ)-induced type 1 diabetic rats. Methods: Lycii Radicis Cortex was orally administered to STZ-induced diabetic rats in doses of 80 or 160 mg/kg body weight/day for 2 weeks, and its effects were compared with those of diabetic control and normal rats. Results: The administration of Lycii Radicis Cortex decreased the elevated serum urea nitrogen and renal reactive oxygen species (ROS), and reduced the increased AGEs in the serum and kidney. The elevated protein expressions of nicotinamide adenine dinucleotide phosphate (NADPH) oxidase subunits in the kidney of diabetic control rats were significantly decreased after Lycii Radicis Cortex treatments. Moreover, the kidney of diabetic rats exhibited the up-regulation of receptor for AGEs (RAGE) and AGEs-related proteins; however, Lycii Radicis Cortex treatment also significantly reduced those expressions (excepted RAGE). In addition, the diabetic rats exhibited an up-regulation of the expression of proteins related to inflammation in the kidney, but Lycii Radicis Cortex administration reduced significantly the expression of the inflammatory proteins through the nuclear factor-kappa B (NF-${\kappa}B$) and activator protein-1 (AP-1) pathways. Conclusions: This study provides scientific evidence that Lycii Radicis Cortex exerts the antidiabetic effect by inhibiting the expressions of AGEs and NF-${\kappa}B$ in the STZ-induced diabetic rats.