ArticleMolecular medicine reports2015
Extract of Rhizoma Polygonum cuspidatum reduces early renal podocyte injury in streptozotocin‑induced diabetic rats and its active compound emodin inhibits methylglyoxal‑mediated glycation of proteins.
Article in Molecular medicine reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 21 citations in OpenAlex.
- Diosmetin Restores Endoplasmic Reticulum Homeostasis to Ameliorate Podocyte Injury in Diabetic Kidney Disease by Targeting DNAJC3.Journal of diabetes research · 2026Article
- Human umbilical cord mesenchymal stem cells attenuate diabetic nephropathy through the IGF1R-CHK2-p53 signalling axis in male rats with type 2 diabetes mellitus.Journal of Zhejiang University. Science. B · 2024Article
- The genusHeliyon · 2024Review
- Research progress of natural active compounds on improving podocyte function to reduce proteinuria in diabetic kidney disease.Renal failure · 2023Review
- Mitochondrial Oxidative Stress and Cell Death in Podocytopathies.Biomolecules · 2022Review
- Recent Advances in Traditional Chinese Medicine for Treatment of Podocyte Injury.Frontiers in pharmacology · 2022Review
- New Approaches on Japanese Knotweed (Plants (Basel, Switzerland) · 2021Review
- Antiglycoxidative Properties of Extracts and Fractions fromNutrients · 2021Article
- Advances in the study of emodin: an update on pharmacological properties and mechanistic basis.Chinese medicine · 2021Review
- Clinical efficacies, underlying mechanisms and molecular targets of Chinese medicines for diabetic nephropathy treatment and management.Acta pharmaceutica Sinica. B · 2021Review
- Cudrania tricuspidata Root Extract Prevents Methylglyoxal-Induced Inflammation and Oxidative Stress via Regulation of the PKC-NOX4 Pathway in Human Kidney Cells.Oxidative medicine and cellular longevity · 2021Article
- Mechanisms and Efficacy of Chinese Herbal Medicines in Chronic Kidney Disease.Frontiers in pharmacology · 2020Review
- Assembly and Annotation of a Draft Genome of the Medicinal PlantFrontiers in plant science · 2019Article
- Article
- GS-E3D, a new pectin lyase-modified red ginseng extract, inhibited diabetes-related renal dysfunction in streptozotocin-induced diabetic rats.BMC complementary and alternative medicine · 2017Article
- Pectin lyase-modified red ginseng extract exhibits potent anti-glycation effects in vitro and in vivo.Journal of exercise nutrition & biochemistry · 2017Article
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5 authors at 1 institution in 1 country.
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Abstract
Podocyte injury contributes to renal damage and, eventually, to the occurrence of proteinuria in diabetic nephropathy. The aim of the present study was to investigate the effect of an ethanol extract from Rhizoma Polygonum cuspidatum (P. cuspidatum) on proteinuria and podocyte injury, and elucidate the underlying mechanism for streptozotocin (STZ)‑induced diabetic nephropathy. The protective effects of P. cuspidatum extract (PCE) on renal podocytes in STZ‑induced diabetic rats were also investigated. PCE (100 or 350 mg/kg/day) was administered to STZ‑induced diabetic rats for 16 weeks, and blood glucose levels, body weight and proteinuria were measured. A double labeling technique with the terminal deoxynucleotidyl transferase dUTP nick end labeling assay was performed and synaptopodin expression was observed. In addition, cleaved caspase‑3, methylglyoxal (MGO) and 8‑hydroxydeoxyguanosine (8‑OHdG) expression levels were measured. STZ‑induced diabetic rats developed hyperglycemia and proteinuria. Increased apoptosis of the podocytes and increased cleaved caspase‑3, MGO and 8‑OHdG expression levels, as well as decreased synaptopodin expression were detected in the glomeruli of STZ‑induced diabetic rats. However, treatment with PCE for 16 weeks restored protein levels to normal, and reduced podocyte loss and apoptosis. Levels of caspase‑3 and MGO expression, as well as oxidative stress were ameliorated by PCE treatment. In addition, emodin, a biologically active ingredient of PCE, exerted an MGO scavenging effect and inhibited MGO‑derived advanced glycation end‑product formation. These findings indicate that PCE may be administered to prevent proteinuria and podocyte loss in STZ‑induced diabetic rats partly by inhibiting podocyte apoptosis and cleaved caspase‑3 expression, and by restoring the balance of oxidative stress and MGO expression.
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