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Chinese journal of integrative medicine ; (12): 910-917, 2016.
Artículo en Inglés | WPRIM | ID: wpr-229541

RESUMEN

<p><b>OBJECTIVE</b>To explore the mechanism of the protective effects of Panax notoginseng saponins (PNS) on kidney in diabetic rats.</p><p><b>METHODS</b>Diabetic rat model was obtained by intravenous injection of alloxan, and the rats were divided into model, PNS-100 mg/(kg day) and PNS-200 mg/(kg day) groups, 10 each. Another 10 rats injected with saline were served as control. Periodic acid-Schiff staining and immunological histological chemistry were used to observe histomorphology and tissue expression of bone morphogenetic protein-7 (BMP-7). Silent information regulator 1 (SIRT1) was silenced in rat mesangial cells by RNA interference. The mRNA expressions of SIRT-1, monocyte chemoattractant protein-1 (MCP-1), transforming growth factor β1 (TGF-β1) and plasminogen activator inhibitor-1 (PAI-1) were analyzed by reverse transcription polymerase chain reaction. The protein expressions of SIRT1 and the acetylation of nuclear factor κB (NF-κB) P65 were determined by western blotting. The concentration of MCP-1, TGF-β1 and malondialdehyde (MDA) in culture supernatant were detected by enzyme-linked immuno sorbent assay. The activity of superoxide dismutase (SOD) was detected by the classical method of nitrogen and blue four.</p><p><b>RESULTS</b>In diabetic model rats, PNS could not only reduce blood glucose and lipid (P<0.01), but also increase protein level of BMP-7 and inhibit PAI-1 expression for suppressing fibrosis of the kidney. In rat mesangial cells, PNS could up-regulate the expression of SIRT1 (P<0.01) and in turn suppress the transcription of TGF-β1 (P<0.05) and MCP-1 (P<0.05). PNS could also reverse the increased acetylation of NF-κB p65 by high glucose. In addition, redox regulation factor MDA was down-regulated (P<0.05) and SOD was up-regulated (P<0.01), which were both induced by SIRT1 up-regulation.</p><p><b>CONCLUSIONS</b>PNS could protect kidney from diabetes with the possible mechanism of up-regulating SIRT1, therefore inhibiting inflammation through decreasing the induction of inflammatory cytokines and TGF-β1, as well as activating antioxidant proteins.</p>


Asunto(s)
Animales , Masculino , Acetilación , Antioxidantes , Metabolismo , Glucemia , Metabolismo , Proteína Morfogenética Ósea 7 , Metabolismo , Quimiocina CCL2 , Metabolismo , Diabetes Mellitus Experimental , Sangre , Quimioterapia , Genética , Técnicas de Silenciamiento del Gen , Inmunohistoquímica , Riñón , Patología , Pruebas de Función Renal , Lípidos , Sangre , Malondialdehído , Metabolismo , Células Mesangiales , Metabolismo , Estrés Oxidativo , Panax notoginseng , Química , Inhibidor 1 de Activador Plasminogénico , Genética , Metabolismo , Sustancias Protectoras , Farmacología , Usos Terapéuticos , Ratas Sprague-Dawley , Saponinas , Farmacología , Usos Terapéuticos , Sirtuina 1 , Genética , Superóxido Dismutasa , Metabolismo , Factor de Transcripción ReIA , Metabolismo , Transcripción Genética , Factor de Crecimiento Transformador beta1 , Metabolismo , Regulación hacia Arriba
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