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Planta Med 2009; 75(11): 1191-1195
DOI: 10.1055/s-0029-1185717
Pharmacology
Original Paper
© Georg Thieme Verlag KG Stuttgart · New York

Salidroside, the Main Active Compound of Rhodiola Plants, Inhibits High Glucose-Induced Mesangial Cell Proliferation

Dengke Yin1 , 2 , Wenbing Yao1 , Song Chen1 , Rongfeng Hu2 , Xiangdong Gao1
  • 1School of Life Science and Technology, China Pharmaceutical University, Nanjing, P. R. China
  • 2School of Pharmacy, Anhui College of Traditional Chinese Medicine, Hefei, P. R. China
Further Information

Publication History

received Dec. 27, 2008 revised March 28, 2009

accepted April 7, 2009

Publication Date:
14 May 2009 (online)

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Abstract

Because Rhodiola plants are known to have a protective effect on diabetic nephropathy, this study aimed to investigate the inhibitory effect of salidroside, the main active component of Rhodiola plants, on high glucose-induced mesangial cell proliferation and its possible mechanism. Salidroside (1 ∼ 100 µM) dose dependently inhibited high glucose-induced mesangial cell early proliferation. Exposure of mesangial cells to high glucose for 24 h significantly induced reactive oxygen species (ROS) accumulation, ERK1/2 phosphorylation, and p27Kip1 expression, and these changes were dramatically inhibited by salidroside in a dose-dependent manner. High glucose-promoted TGF-β1 secretion was also significantly attenuated by treatment of mesangial cells with salidroside. These results indicated that salidroside had the ability to inhibit high glucose-induced mesangial cell proliferation, which is in correlation with salidroside suppressing TGF-β1 production and ERK1/2 phosphorylation.

Key words

salidroside - high glucose - proliferation - TGF‐β1 - ERK1/2 - Rhodiola (Crassulaceae)

References

  • 1 Yamagishi S, Fukami K, Ueda S, Okuda S. Molecular mechanisms of diabetic nephropathy and its therapeutic intervention.  Curr Drug Targets. 2007;  8 952-959
    CrossrefPubMedSearch in Google Scholar
  • 2 Mahadevan P, Larkins R G, Fraser J R, Dunlop M E. Effect of prostaglandin E2 and hyaluronan on mesangial cell proliferation. A potential contribution to glomerular hypercellularity in diabetes.  Diabetes. 1996;  45 44-50
    CrossrefPubMedSearch in Google Scholar
  • 3 Young B A, Johnson R L, Alpers C E, Eng E, Gordon K, Floege J, Couser W G, Seidel K. Cellular events in the evolution of experimental diabetic nephropathy.  Kidney Int. 1995;  47 935-944
    CrossrefPubMedSearch in Google Scholar
  • 4 Kurogi Y. Mesangial cell proliferation inhibitors for the treatment of proliferative glomerular disease.  Med Res Rev. 2003;  23 15-31
    CrossrefPubMedSearch in Google Scholar
  • 5 Wolf G, Sharma K, Chen Y, Ericksen M, Ziyadeh F N. High glucose-induced proliferation in mesangial cells is reversed by autocrine TGF-β.  Kidney Int. 1992;  42 647-656
    CrossrefPubMedSearch in Google Scholar
  • 6 Kreisberg J I, Radnik R A, Ayo S H, Garoni J, Saikumar P. High glucose elevates c-fos and c-jun transcripts and proteins in mesangial cell cultures.  Kidney Int. 1994;  46 105-112
    CrossrefPubMedSearch in Google Scholar
  • 7 Shankland S J, Scholey J W. Expression of growth-related protooncogenes during diabetic renal hypertrophy.  Kidney Int. 1995;  47 782-788
    CrossrefPubMedSearch in Google Scholar
  • 8 Wolf G, Schroeder R, Ziyadeh F N, Thaiss F, Zahner G, Stahl R A. High glucose stimulates expression of p 27Kip1 in cultured mouse mesangial cells: relationship to hypertrophy.  Am J Physiol. 1997;  273 348-356
    PubMedSearch in Google Scholar
  • 9 Choi H T, Cui C B, Kim S H, Ham Y A, Lee D S, Ham S S. Effects of Rhodiola sachalinensis extract in streptozotocin-induced diabetic rats.  East Asian Soc Dietary Life. 2005;  15 158-164
    PubMedSearch in Google Scholar
  • 10 Kim S H, Hyun S H, Choung S Y. Antioxidative effects of Cinnamomi cassiae and Rhodiola rosea extracts in liver of diabetic mice.  Biofactors. 2006;  26 209-219
    CrossrefPubMedSearch in Google Scholar
  • 11 Kucinskaite A, Poblocka-Olech L, Krauze-Baranowska M, Sznitowska M, Savickas A, Briedise V. Evaluation of biologically active compounds in roots and rhizomes of Rhodiola rosea L. cultivated in Lithuania.  Medcina. 2007;  43 487-494
    PubMedSearch in Google Scholar
  • 12 Nakamura S, Li X, Matsuda H, Ninomiya K, Morikawa T, Yamaguti K, Yoshikawa M. Bioactive constituents from Chinese natural medicines. XXVI. Chemical structures and hepatoprotective effects of constituents from roots of Rhodiola sachalinensis.  Chem Pharm Bull. 2007;  55 1505-1511
    CrossrefPubMedSearch in Google Scholar
  • 13 Li H B, Ge Y, Zheng X X, Zhang L. Salidroside stimulated glucose uptake in skeletal muscle cells by activating AMP-activated protein kinase.  Eur J Pharmacol. 2008;  588 165-169
    CrossrefPubMedSearch in Google Scholar
  • 14 Ruan X Z, Varghese Z, Powis S H, Moorhead J F. Dysregulation of LDL receptor under the influence of inflammatory cytokines: a new pathway for foam cell formation.  Kidney Int. 2001;  60 1716-1725
    CrossrefPubMedSearch in Google Scholar
  • 15 Sraer J D, Delarue F, Hagege J, Feunteun J, Pinet F, Nguyen G, Rondeau E. Stable cell lines of T-SV40 immortalized human glomerular mesangial cell.  Kidney Int. 1996;  49 267-270
    CrossrefPubMedSearch in Google Scholar
  • 16 Nahman Jr N S, Leonhart K L, Cosio F G, Hebert C L. Effects of high glucose on cellular proliferation and fibronectin production by cultured human mesangial cells.  Kidney Int. 1992;  41 396-402
    CrossrefPubMedSearch in Google Scholar
  • 17 Mason R M, Wahab N A. Extracellular matrix metabolism in diabetic nephropathy.  J Am Soc Nephrol. 2003;  14 1358-1373
    CrossrefPubMedSearch in Google Scholar
  • 18 Wolf G, Shankland S J. Cell cycle control in glomerular disease.  Prog Cell Cycle Res. 2003;  5 71-79
    PubMedSearch in Google Scholar
  • 19 Rosen L B, Ginty D D, Greenberg M E. Calcium regulation of gene expression.  Adv Second Messenger Phosphoprotein Res. 1995;  30 225-253
    PubMedSearch in Google Scholar
  • 20 Ziyadeh F N. Mediators of diabetic renal disease: the case for TGF-beta as the major mediator.  J Am Soc Nephrol. 2004;  15 S55-S57
    CrossrefPubMedSearch in Google Scholar
  • 21 Sharma K, Jin Y, Guo J, Ziyadeh F N. Neutralization of TGF-β by anti-TGF-β antibody attenuates kidney hypertrophy and the enhanced extracellular matrix gene expression in streptozotocin-induced diabetic mice.  Diabetes. 1996;  45 522-530
    CrossrefPubMedSearch in Google Scholar
  • 22 Kolm V, Sauer U, Olegomoller B, Scheicher E D. High-glucose-induced TGF-β1 regulates mesangial production of heparan sulfate proteoglycan.  Am J Physiol. 1996;  270 F812-F821
    PubMedSearch in Google Scholar
  • 23 Chen S, Iglesias-de la Cruz M C, Jim B, Hong S W, Isono M, Ziyadeh F N. Reversibility of established diabetic glomerulopathy by anti-TGF-beta antibodies in db/db mice.  Biochem Biophys Res Commun. 2003;  300 16-22
    CrossrefPubMedSearch in Google Scholar

Prof. Dr. Xiangdong Gao

School of Life Science and Technology
China Pharmaceutical University

24 Tongjia Road

Nanjing 210009

People's Republic of China

Phone: + 86 25 83 27 12 98

Fax: + 86 25 83 27 12 49

Email: xiangdon_gao@hotmail.com