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KMID : 0525720210260040178
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Journal of Chitin and Chitosan
2021 Volume.26 No. 4 p.178 ~ p.186
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Gelidium amansii Extract Alleviates Advanced Glycation-End Products-Induced Diabetic Nephropathy in Mouse Glomerular Mesangial Cells
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Cho Chi-Heung
Kim Min-Gyeong
Kim Se-Ra
Lee Sang-Hoon
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Abstract
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In this study, we evaluated the anti-glycation activity and nephroprotective effects of Gelidium amansii 70% (v/v) ethanol extract (GAE) in mouse glomerular mesangial cells. GAE (1, 5, and 20 μg/mL) treatment significantly reduced advanced glycation end-products (AGEs) formation (p < 0.001), and inhibited AGEs formation up to 47.8% at 1 μg/mL GAE. In addition, GAE not only significantly inhibited the formation of AGEs-collagen cross-linking, but also showed the effect of breaking the already formed cross-links (p < 0.001). In particular, 20 μg/mL GAE (41.9%) exhibited similar breaking ability as ALT-711 (0.5 mg/mL, 33.7%) used as a positive control. Treatment of methylglyoxal (MGO), a precursor of AGEs, on mouse glomerular mesangial cells, increased intracellular MGO and AGEs accumulation, leading to increased reactive oxygen species (ROS) production and eventually induced renal cell apoptotic death. However, pre-treatment with the GAE, at 1, 5 and 20 μg/mL, reduced intracellular ROS production level to approximately 541.1-201.4%. Especially, pre-treatment of 20 μg/mL GAE significantly decreased intracellular MGO concentration (18.99 μg/mL) to a level similar to that of the non-treated group (16.67 μg/mL) (p < 0.001). Moreover, it was confirmed by immunofluorescence analysis that GAE suppressed the AGEs accumulation in mouse glomerular mesangial cells. As a result, due to this effects of GAE, MGO-induced apoptotic cell death was dramatically reduced, proving that GAE has an ability in preventing AGEs-related diabetic nephropathy. Therefore, our results suggest that Gelidium amansii has high potential to be developed as a natural agent for diabetic complications with a low risk of side effects.
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KEYWORD
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Gelidium amansii, Anti-glycation activity, Advanced glycation end-product, Nephroprotective effect, Apoptosis
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