Effects of Panax notoginoside on the expression of TGF-β1 and Smad-7 in renal tissues of diabetic rats

Qingnian Tu , Juan Qin , Hui Dong , Fuer Lu , Wei Guan

Current Medical Science ›› 2011, Vol. 31 ›› Issue (2)

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Current Medical Science ›› 2011, Vol. 31 ›› Issue (2) DOI: 10.1007/s11596-011-0250-5
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Effects of Panax notoginoside on the expression of TGF-β1 and Smad-7 in renal tissues of diabetic rats

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Abstract

In order to explore the effects of Panax notoginoside (PNS) on the expression of transforming growth factor β1 (TGF-β1) and Smad-7 in renal tissues of diabetes, a rat model of diabetic nephropathy was set up by intravenous injection of streptozotocin (STZ). Wistar rats were randomly divided into normal group, diabetic control group, group treated by PNS at low-dosage (PL), group treated by PNS at high-dosage (PH) and group treated by catopril (C), respectively. Fasting blood glucose (FBG), renal index, endogenous creatinine clearance rate (CCr) and urinary albumin (UAlb) in 24 h were examined after 6 weeks. Meanwhile, the expressions of TGF-β1 and Smad7 in renal tissues were immunohistochemically dectected. At the end of the sixth week, FBG, renal index, Ccr, UAlb were all elevated significantly in control group (P<0.01). The expression of TGF-β1 protein was increased while Smad7 protein decreased in renal tissue (P<0.01). However, the treatment with PNS reversed the aforementioned changes in renal tissues of diabetic rats. These results indicate that PNS possess a protective effect on the kidney of diabetic rats and it might protect kidney by inhibiting the expression of TGF-β1 protein and enhancing the expression of Smad7 protein.

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Panax notoginoside / diabetes / TGF-β1 / Smad-7

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Qingnian Tu, Juan Qin, Hui Dong, Fuer Lu, Wei Guan. Effects of Panax notoginoside on the expression of TGF-β1 and Smad-7 in renal tissues of diabetic rats. Current Medical Science, 2011, 31(2): DOI:10.1007/s11596-011-0250-5

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References

[1]

KikkawaR., TogawaM., IsonoM., et al.. Mechanism of the progression of diabetic nephropathy to renal failure. Kidney Int Suppl, 1997, 62: S39-S40

[2]

DerynckR., ZhangY.E.. Smad-dependent and Smad-independent pathways in TGF-beta family signalling. Nature, 2003, 425(6958): 577-584

[3]

KavsakP., RasmussenR.K., CausingC.G., et al.. Smad7 binds to Smurf2 to form an E3 ubiquitin ligase that targets the TGF-beta receptor for degradation. Mol Cell, 2000, 6(6): 1365-1375

[4]

SchifferM., SchifferL.E., GuptaA., et al.. Inhibitory smads and TGF-beta signaling in glomerular cells. J Am Soc Nephrol, 2002, 13(11): 2657-2666

[5]

Tu QN, Dong H, Lu FE. Effects of Panax Notoginoside on the nephropathy in rats with type 1 diabetes. Chin J Integr Med, 2011 (in press).

[6]

ChenW.B., PanX.L.. . Diagnostics (sixth edition), 2003, Beijing, People’s Medical Publishing House, 379-380

[7]

RaptisA.E., VibertiG.. Pathogenesis of diabetic nephropathy. Exp Clin Endocrinol Diabetes, 2001, 109(Suppl2): S424-S437

[8]

DronavalliS., DukaI., BakrisG.L.. The pathogenesis of diabetic nephropathy. Nat Clin Pract Endocrinol Metab, 2008, 4(8): 444-452

[9]

LangJ., CaoH., WeiA.. Comparative study on effect of Panax notoginseng and ticlid in treating early diabetic nephropathy. Zhongguo Zhong Xi Yi Jie He Za Zhi (Chinese), 1998, 18(12): 727-729

[10]

ChenZ.H., LiJ., LiuJ., et al.. Saponins isolated from the root of Panax notoginseng showed significant anti-diabetic effects in KK-Ay mice. Am J Chin Med, 2008, 36(5): 939-951

[11]

GuoM., LiuH., ChenXw.. The mechanisms of progression of renal interstitial fibrosis and the therapeutic effects of Panax notoginoside. Zhongguo Zhong Xi Yi Jie He Shen Bing Za Zhi (Chinese), 2007, 8(3): 175-178

[12]

WangW., KokaV., LanH.Y.. Transforming growth factor-β and Smad signaling in kidney diseases. Nephrology, 2005, 10(1): 48-56

[13]

OkazakiY., YamasakiY., UchidaH.A., et al.. Enhanced TGF-β/Smad signaling in the early stage of diabetic nephropathy is independent of the AT1a receptor. Clin and Exper Nephrol, 2007, 11(1): 77-87

[14]

HillsC.E., SquiresP.E.. TGF-beta1-induced epithelial-to-mesenchymal transition and therapeutic intervention in diabetic nephropathy. Am J Nephrol, 2010, 31(1): 68-74

[15]

LapingN.J., GrygielkoE., MathurA., et al.. Inhibition of transforming growth factor (TGF)-β1-induced extracellular matrix with a novel inhibitor of the TGF-β type I receptor kinase activity: SB-431542. Mol Pharmacol, 2002, 62(1): 58-64

[16]

LiJ., KangS.W., KimJ.L., et al.. Isoliquiritigenin entails blockade of TGF-beta1-Smad signaling for retarding high glucose-induced mesangial matrix accumulation. J Agric Food Chem, 2010, 58(5): 3205-32121

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