ArticleJournal of Korean medical science2011
Ginseng total saponin improves podocyte hyperpermeability induced by high glucose and advanced glycosylation endproducts.
Article in Journal of Korean medical science, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 15 citations in OpenAlex.
- Preventive effect of Korean red ginseng for acute respiratory illness: a randomized and double-blind clinical trial.Journal of Korean medical science · 2012Trial
- TCM-based natural products in type 2 diabetes: a comprehensive review of bioactive compounds and molecular mechanisms.Molecular diversity · 2026Review
- Piperazine ferulate prevents high-glucose-induced filtration barrier injury of glomerular endothelial cells.Experimental and therapeutic medicine · 2021Article
- Montelukast improves the changes of cytoskeletal and adaptor proteins of human podocytes by interleukin-13.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2017Article
- Effects of interleukin-13 and montelukast on the expression of zonula occludens-1 in human podocytes.Yonsei medical journal · 2015Article
- Ginseng total saponin modulates the changes of α-actinin-4 in podocytes induced by diabetic conditions.Journal of ginseng research · 2014Article
- Saponin as regulator of biofuel: implication for ethnobotanical management of diabetes.Journal of physiology and biochemistry · 2014Review
- Ginseng total saponin modulates podocyte p130Cas in diabetic condition.Journal of ginseng research · 2013Article
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Authors and funding
4 authors at 1 institution in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
Early diabetic nephropathy is characterized by glomerular hyperpermeability as a result of impaired glomerular filtration structure caused by hyperglycemia, glycated proteins or irreversible advanced glycosylation endproducts (AGE). To investigate the effect of ginseng total saponin (GTS) on the pathologic changes of podocyte ZO (zonula occludens)-1 protein and podocyte permeability induced by diabetic conditions, we cultured mouse podocytes under: 1) normal glucose (5 mM, = control); 2) high glucose (HG, 30 mM); 3) AGE-added; or 4) HG plus AGE-added conditions and treated with GTS. HG and AGE increased the dextran filtration of monolayered podocytes at early stage (2-8 hr) in permeability assay. In confocal imaging, ZO-1 colocalized with actin filaments and β-catenin at cell contact areas, forming intercellular filtration gaps. However, these diabetic conditions suppressed ZO-1 immunostainings and disrupted the linearity of ZO-1. In Western blotting, diabetic conditions also decreased cellular ZO-1 protein levels at 6 hr and 24 hr. GTS improved such quantitative and qualitative changes. These findings imply that HG and AGE have an influence on the redistribution and amount of ZO-1 protein of podocytes thereby causing hyperpermeability at early stage, which can be reversed by GTS.
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