Therapeutic Potential of Phlorotannin-Rich Ecklonia cava Extract on Methylglyoxal-Induced Diabetic Nephropathy in In Vitro Model

Advanced glycation end-products (AGEs) play a vital role in the pathogenesis of diabetic complications. Methylglyoxal (MGO), one of the major precursors of AGEs, is a highly reactive dicarbonyl compound that plays an important role in the pathogenesis of diabetic nephropathy. This study was designed...

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Bibliographic Details
Published in:Marine drugs 2022-05, Vol.20 (6), p.355
Main Authors: Cho, Chi-Heung, Lee, Chang-Jun, Kim, Min-Gyeong, Ryu, Bomi, Je, Jun-Geon, Kim, Yoonsook, Lee, Sang-Hoon
Format: Article
Language:English
Subjects:
Accumulation
advanced glycation end-products
Advanced glycosylation end products
Age
Animal models
Antioxidants
Apoptosis
Carbonyl compounds
Collagen
Cross-linking
Crosslinking
Damage accumulation
Diabetes
Diabetes mellitus
Diabetic nephropathy
Ecklonia cava
Enzymes
GA-binding protein
Glycosylation
Intracellular
Intracellular signalling
Mesangial cells
methylglyoxal
mouse glomerular mesangial cell
Nephropathy
Oxidative stress
Pathogenesis
phlorotannin
Properties
Protein adducts
Proteins
Pyruvaldehyde
Reactive oxygen species
Signal transduction
Signaling
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Summary:Advanced glycation end-products (AGEs) play a vital role in the pathogenesis of diabetic complications. Methylglyoxal (MGO), one of the major precursors of AGEs, is a highly reactive dicarbonyl compound that plays an important role in the pathogenesis of diabetic nephropathy. This study was designed to evaluate the therapeutic potential of phlorotannin-rich Ecklonia cava extract (ECE) on MGO-induced diabetic nephropathy in in vitro models using mouse glomerular mesangial cells. ECE showed anti-glycation activity via breaking of AGEs-collagen cross-links and inhibition of AGEs formation and AGE-collagen cross-linking formation. The renoprotective effects were determined by assessing intracellular reactive oxygen species (ROS) and MGO accumulation, cell apoptosis, and the Nrf-2/ARE signaling pathway. MGO-induced renal damage, intracellular ROS production level, and MGO-protein adduct accumulation were significantly decreased by pretreating ECE. Moreover, ECE pretreatment exhibited preventive properties against MGO-induced dicarbonyl stress via activation of the Nrf2/ARE signaling pathway and reduction of RAGE protein expression in mouse glomerular mesangial cells. Collectively, these results indicated potential anti-glycation properties and prominent preventive effects of ECE against MGO-induced renal damage. Additionally, ECE may be utilized for the management of AGE-related diabetic nephropathy.
ISSN:1660-3397
1660-3397
DOI:10.3390/md20060355