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EGCG ‐rich green tea extract stimulates s RAGE secretion to inhibit S 100 A 12‐ RAGE axis through ADAM 10‐mediated ectodomain shedding of extracellular RAGE in type 2 diabetes
Author(s) -
Huang ShangMing,
Chang YinHsuan,
Chao YaChan,
Lin JerAn,
Wu ChiHao,
Lai ChingYi,
Chan KungChi,
Tseng ShihTing,
Yen GowChin
Publication year - 2013
Publication title -
molecular nutrition and food research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.495
H-Index - 131
eISSN - 1613-4133
pISSN - 1613-4125
DOI - 10.1002/mnfr.201300275
Subject(s) - rage (emotion) , chemistry , secretion , microbiology and biotechnology , biochemistry , biology , neuroscience
The receptor for advanced glycation of end products ( RAGE ) plays a critical role in the progression of type 2 diabetes ( T 2 D ). Soluble RAGE (s RAGE ) is one of the RAGE variants, which acts as a decoy domain receptor and competes with RAGE , thus contributing to prevention of T 2 D . In this study, we conducted clinical trials of (–)‐epigallocatechin‐3‐gallate ( EGCG ) rich green tea extract (300–900 mg/day) to investigate the effect of EGCG on relationship between S 100 A 12 RAGE ligand and diverse s RAGE in T 2 D . Moreover, mechanism of s RAGE production also confirmed in vitro. Our data indicated that EGCG could stimulate s RAGE circulation but inhibited RAGE ligand in T 2 D , and ADAM 10‐mediated ectodomain shedding of extracellular RAGE was mainly involved in EGCG ‐stimulated s RAGE circulation. The present evidence indicates that EGCG has a potential to block S100A12‐ RAGE axis by stimulating s RAGE production through ADAM 10‐mediated ectodomain shedding of extracellular RAGE . Therefore, EGCG contributes to nutritional strategies for diabetes, not only because of its efficient antioxidant activity to scavenge free radicals, but also because of its ability stimulating s RAGE release in the circulation. Additionally, ADAM 10‐induced ectodomain shedding of extracellular RAGE leading to s RAGE circulation should be a potential of passive mechanism of s RAGE production to block S 100 A 12‐ RAGE axis‐related pathogenesis of proinflammation and diabetes.