AGEs are a heterogeneous group of non-enzymatically glycated molecules, especially proteins or lipids, usually resulting in fluorescent derivatives. Endogenous AGE formation naturally occurs during aging or in conditions of chronic hyperglycemia and oxidative stress, whereas intake of exogenous AGEs is linked to food consumption in Western diets (1). AGE accumulation in muscle, blood and skin is associated with reduced muscle mass (atrophy) and strength, and AGEs induce atrophy per se by interaction with the receptor for advanced glycation end-products (RAGE) (2). We tested thirty standardized dry extracts (from officinal plants and mushrooms), purified active compounds, and a food supplement (KYMASIN UP) for their ability in counteracting glyceraldehyde-derived fluorescent AGE formation by using a well-characterized albumin glycation assay kit (3), in which aminoguanidine solution was used as an anti-AGEs control. We found that: i) seven herbal extracts (Withania somnifera, Equisetum arvense, Vaccinium macrocarpon, Euterpe oleracea, Camellia sinensis, Rhodiola rosea, Lepidium meyenii), a mushroom (Cordyceps sinensis), three active compounds (lycopene, alpha lipoic acid, chlorophyll), and KYMASIN UP were able to inhibit AGE formation (fluorescence intensity) at 100 μg/ml in 24h; ii) V. macrocarpon, Camellia sinensis and chlorophyll showed a surprising ability in counteracting AGE formation in a dose-dependent manner starting from 3h; and iii) Camellia sinensis 500 μg/ml completely abolished AGE-derived fluorescence starting from 6h. Thus, we have identified natural products able to prevent AGE formation/accumulation to be tested in in vitro and in vivo experimental models of muscle atrophy for their potential in reducing the AGE-dependent detrimental effects in muscles. 1. Perrone A. et al., Oxid Med Cell Longev. 2020, 18;2020:3818196; 2. Suzuki A. et al., Methods. 2020, 203:179-186; 3. Takino J. et al., J Gastroenterol. 2010, 45(6):646-55.
Identification of natural products able to counteract the formation of advanced glycation end-products (AGEs) sustaining muscle atrophy
Salvadori L.;Bellomo G.;Chiappalupi S.;Gentili G.;Sorci G.;Riuzzi F
2022
Abstract
AGEs are a heterogeneous group of non-enzymatically glycated molecules, especially proteins or lipids, usually resulting in fluorescent derivatives. Endogenous AGE formation naturally occurs during aging or in conditions of chronic hyperglycemia and oxidative stress, whereas intake of exogenous AGEs is linked to food consumption in Western diets (1). AGE accumulation in muscle, blood and skin is associated with reduced muscle mass (atrophy) and strength, and AGEs induce atrophy per se by interaction with the receptor for advanced glycation end-products (RAGE) (2). We tested thirty standardized dry extracts (from officinal plants and mushrooms), purified active compounds, and a food supplement (KYMASIN UP) for their ability in counteracting glyceraldehyde-derived fluorescent AGE formation by using a well-characterized albumin glycation assay kit (3), in which aminoguanidine solution was used as an anti-AGEs control. We found that: i) seven herbal extracts (Withania somnifera, Equisetum arvense, Vaccinium macrocarpon, Euterpe oleracea, Camellia sinensis, Rhodiola rosea, Lepidium meyenii), a mushroom (Cordyceps sinensis), three active compounds (lycopene, alpha lipoic acid, chlorophyll), and KYMASIN UP were able to inhibit AGE formation (fluorescence intensity) at 100 μg/ml in 24h; ii) V. macrocarpon, Camellia sinensis and chlorophyll showed a surprising ability in counteracting AGE formation in a dose-dependent manner starting from 3h; and iii) Camellia sinensis 500 μg/ml completely abolished AGE-derived fluorescence starting from 6h. Thus, we have identified natural products able to prevent AGE formation/accumulation to be tested in in vitro and in vivo experimental models of muscle atrophy for their potential in reducing the AGE-dependent detrimental effects in muscles. 1. Perrone A. et al., Oxid Med Cell Longev. 2020, 18;2020:3818196; 2. Suzuki A. et al., Methods. 2020, 203:179-186; 3. Takino J. et al., J Gastroenterol. 2010, 45(6):646-55.I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.
