ArticleInternational journal of molecular medicine2016
Notoginsenoside R1 ameliorates podocyte injury in rats with diabetic nephropathy by activating the PI3K/Akt signaling pathway.
Article in International journal of molecular medicine, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers, 2 of them syntheses that pooled it.
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Who cites it
35 citing papers in PubMed, 2 syntheses or guidelines pooled it, 67 citations in OpenAlex.
- The effects of Panax notoginseng for the treatment of diabetic nephropathy in animals: a systematic review and meta-analysis.Frontiers in nutrition · 2026Pooled it
- Pooled it
- Therapeutic role of Crateva religiosa in diabetic nephropathy: Insights into key signaling pathways.PloS one · 2025Article
- Pharmacological potential of Chinese botanical drugs in managing chronic kidney disease by targeting mitochondrial quality control.Frontiers in pharmacology · 2025Review
- Ginsenoside in the treatment of type 2 diabetes and its complications: a promising traditional chinese medicine.Frontiers in pharmacology · 2025Review
- Unlocking the mechanistic potential ofJournal of traditional and complementary medicine · 2024Review
- Bidirectional two-sample Mendelian randomization analysis unveils causal association between inflammatory cytokines and the risk of diabetic nephropathy.Scientific reports · 2024Article
- The role of PI3K/Akt signaling pathway in chronic kidney disease.International urology and nephrology · 2024Review
- Notoginsenoside R1, a metabolite from Panax notoginseng (Burkill) F.H.Chen, stimulates insulin secretion through activation of phosphatidylinositol 3-kinase (PI3K)/Akt pathway.Frontiers in pharmacology · 2024Article
- Jiawei Shengjiangsan's Effect on Renal Injury in Diabetic Nephropathy Mice is Investigated via the PI3K/Akt/NF-κB Signaling Pathway.Diabetes, metabolic syndrome and obesity : targets and therapy · 2024Article
- Association of inflammatory cytokines with type 2 diabetes mellitus and diabetic nephropathy: a bidirectional Mendelian randomization study.Frontiers in medicine · 2024Article
- Network pharmacology and molecular docking technology-based predictive study of the active ingredients and potential targets of rhubarb for the treatment of diabetic nephropathy.BMC complementary medicine and therapies · 2022Article
- The role of extracellular vesicles in podocyte autophagy in kidney disease.Journal of cell communication and signaling · 2021Review
- Transforming growth factor-β1-induced podocyte injury is associated with increased microRNA-155 expression, enhanced inflammatory responses and MAPK pathway activation.Experimental and therapeutic medicine · 2021Article
- Construction and Bioinformatics Analysis of the miRNA-mRNA Regulatory Network in Diabetic Nephropathy.Journal of healthcare engineering · 2021Article
- Notoginsenoside R1 Protects Against High Glucose-Induced Cell Injury Through AMPK/Nrf2 and Downstream HO-1 Signaling.Frontiers in cell and developmental biology · 2021Article
- Total Flavones ofFrontiers in pharmacology · 2021Article
- Network Pharmacology Combined with Bioinformatics to Investigate the Mechanisms and Molecular Targets ofEvidence-based complementary and alternative medicine : eCAM · 2021Article
- Artesunate Combined With Metformin Ameliorate on Diabetes-Induced Xerostomia by Mitigating Superior Salivatory Nucleus and Salivary Glands Injury in Type 2 Diabetic Rats via the PI3K/AKT Pathway.Frontiers in pharmacology · 2021Article
- Protosappanin-A and oleanolic acid protect injured podocytes from apoptosis through inhibition of AKT-mTOR signaling.Cell biology international · 2020Article
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Authors and funding
11 authors at 4 institutions in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
The present study was designed to examine the protective effect of notoginsenoside R1 (NR1) on podocytes in a rat model of streptozotocin (STZ)‑induced diabetic nephropathy (DN), and to explore the mechanism responsible for NR1-induced renal protection. Diabetes was induced by a single injection of STZ, and NR1 was administered daily at a dose of 5 mg/kg (low dose), 10 mg/kg (medium) and 20 mg/kg (high) for 16 weeks in Sprague-Dawley rats. Blood glucose levels, body weight and proteinuria were measured every 4 weeks, starting on the day that the rats received NR1. Furthermore, on the day of sacrifice, blood, urine and kidneys were collected in order to assess renal function according to general parameters. Pathological staining was performed to evaluate the renal protective effect of NR1, and the expression of the key slit diaphragm proteins, namely neprhin, podocin and desmin, were evaluated. In addition, the serum levels of inflammatory cytokines [tumor necrosis factor-α (TNF-α), tumor growth factor-β1 (TGF-β1), interleukin (IL)-1 and IL-6] as well as an anti-inflammatory cytokine (IL-10) were assessed, and the apoptosis of podocytes was quantified. Finally, the phosphoinositide 3-kinase (PI3K)/Akt signaling pathway and the involvement of nuclear factor-κB (NF-κB) inactivation was further analyzed. In this study, NR1 improved renal function by ameliorating histological alterations, increasing the expression of nephrin and podocin, decreasing the expression of desmin, and inhibiting both the inflammatory response as well as the apoptosis of podocytes. Furthermore, NR1 treatment increased the phosphorylation of both PI3K (p85) and Akt, indicating that activation of the PI3K/Akt signaling pathway was involved. Moreover, NR1 treatment decreased the phosphorylation of NF-κB (p65), suggesting the downregulation of NF-κB. This is the first study to the best of our knowledge, to clearly demonstrate that NR1 treatment ameliorates podocyte injury by inhibiting both inflammation and apoptosis through the PI3K/Akt signaling pathway.
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