Objective: To explore the mechanism of the protective effects of Panax notoginseng saponins(PNS) on kidney in diabetic rats. Methods: Diabetic rat model was obtained by intravenous injection of alloxan, and the ra...Objective: To explore the mechanism of the protective effects of Panax notoginseng saponins(PNS) on kidney in diabetic rats. Methods: 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 mR NA 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. Results: 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. Conclusions: 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.展开更多
基金Supported by National Natural Science Foundation of China(No.81273615)Zhejiang Provincial Natural Science Fund(No.Y2110849)
文摘Objective: To explore the mechanism of the protective effects of Panax notoginseng saponins(PNS) on kidney in diabetic rats. Methods: 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 mR NA 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. Results: 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. Conclusions: 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.