ArticleAmerican journal of translational research2017
Nicousamide protects kidney podocyte by inhibiting the TGFβ receptor II phosphorylation and AGE-RAGE signaling.
Article in American journal of translational research, 2017. 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.
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- Dynamic gut microbiome-metabolome in cationic bovine serum albumin induced experimental immune-complex glomerulonephritis and effect of losartan and mycophenolate mofetil on microbiota modulation.Journal of pharmaceutical analysis · 2024Article
- Investigating the Molecular Mechanism of Quercetin Protecting against Podocyte Injury to Attenuate Diabetic Nephropathy through Network Pharmacology, MicroarrayData Analysis, and Molecular Docking.Evidence-based complementary and alternative medicine : eCAM · 2022Article
- Knockout of NGAL aggravates tubulointerstitial injury in a mouse model of diabetic nephropathy by enhancing oxidative stress and fibrosis.Experimental and therapeutic medicine · 2021Article
- An Overview of the Posttranslational Modifications and Related Molecular Mechanisms in Diabetic Nephropathy.Frontiers in cell and developmental biology · 2021Review
- Renoprotective effect of vildagliptin following hepatic ischemia/reperfusion injury.Renal failure · 2020Article
- Liraglutide inhibits the apoptosis of human nucleus pulposus cells induced by high glucose through PI3K/Akt/caspase-3 signaling pathway.Bioscience reports · 2019Article
- The aqueous extract of Lycopus lucidus Turcz exerts protective effects on podocytes injury of diabetic nephropathy via inhibiting TGF-β1 signal pathway.American journal of translational research · 2019Article
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Authors and funding
7 authors.
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Abstract
Nicousamide, a clinical phase II renal protective new drug, has been demonstrated to have renal protective effect on diabetic nephropathy (DN) by experimental animal model. Its known molecular mechanisms include AGE formation blocking and moderately decreasing the blood pressure. Nicousamide shows potential on attenuating albuminuria, thereby suggests it might have protective effect on podocytes. The aim of present study was to investigate whether nicousamide could protect integrity of podocytes, and further its protection mechanisms. Sprague-Dawley (SD) rats were induced to DN by streptozotocin, and nicousamide (20 and 40 mg/kg) was orally administrated for 20 weeks. Every five weeks, the albuminuria was measured, and renal pathology was evaluated at the end of experiment. Real-time PCR and immunofluorescence were used to test expression of podocyte marker nephrin, CD2AP and podocine in rat kidney tissues. Western blot was used to test the activation and phosphorylation of TGFβ1-smad signaling pathway. surface plasmon resonance (SPR) technology was used to analyze whether nicousamide can interact with TGFβ1 receptor II (TGFβ RII) and receptor for advanced glycation endproducts (RAGE). Results demonstrate that nicousamide significantly reduces albuminuria and ameliorate the glomerulosclerosis in DN rats. RT-PCR and immunofluorescence demonstrate that nicousamide can increase the expression of podocyte markers and keep podocyte effacement. Phosphorylation of TGFβ RII and smad2 in rat kidney was inhibited by nicousamide dose dependently. SPR demonstrate that nicousamide have strong binding capability with hRAGE with Kd approximate 6 μM. These results indicate a protective effect of nicousamide against podocyte injury, and this effect might contribute from suppression of TGFβ-involved fibrosis and AGE-RAGE signaling activation.
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28123638PMC5250708What OpenQuestion holds
Registered trials
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