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Pectin lyase-modified red ginseng extract exhibits potent anti-glycation effects in vitro and in vivo

[PURPOSE]: GS-E3D is a newly developed pectin lyase-modified red ginseng extract. The purpose of this study was to evaluate the inhibitory effects of GS-E3D against advanced glycation end products. [METHODS]: In this study, we evaluated the inhibitory effects of GS-E3D on the formation of advanced g...

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Detalles Bibliográficos
Autores principales: Kim, Chan-Sik, Jo, Kyuhyung, Pyo, Mi-Kyung, Kim, Jin Sook, Kim, Junghyun
Formato: Online Artículo Texto
Lenguaje:English
Publicado: 한국운동영양학회 2017
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5545198/
https://www.ncbi.nlm.nih.gov/pubmed/28715887
http://dx.doi.org/10.20463/jenb.2017.0011
Descripción
Sumario:[PURPOSE]: GS-E3D is a newly developed pectin lyase-modified red ginseng extract. The purpose of this study was to evaluate the inhibitory effects of GS-E3D against advanced glycation end products. [METHODS]: In this study, we evaluated the inhibitory effects of GS-E3D on the formation of advanced glycation end products (AGEs) and their cross-linking with collagen in vitro and in streptozotocin-induced diabetic rats. [RESULTS]: An in vitro assay for the glycation of bovine serum albumin by methylglyoxal showed that GS-E3D inhibited AGE formation at an IC50 value of 19.65 ± 4.35 μg/mL. In addition, GS-E3D showed a potent inhibitory effect (IC50 = 0.42 ± 0.08 mg/mL) on the cross-linking of AGEs with collagen. However, GS-E3D showed no effect on preformed AGEs cross-linked with collagen in the breakdown assay. To determine whether GS-E3D inhibits AGE formation and their cross-linking with proteins in vivo, streptozotocin induced diabetic rats were treated with GS-E3D (25, 50, and 100 mg/kg/day) for 6 weeks. The administration of GS-E3D decreased serum levels of AGEs and their cross linking with proteins in diabetic rats. [CONCLUSION]: The inhibitory effects of this agent on advanced glycation in vitro and in vivo suggested that it may have a potential therapeutic role in controlling diabetes-induced AGE burden in various tissues.