ASN's Mission

To create a world without kidney diseases, the ASN Alliance for Kidney Health elevates care by educating and informing, driving breakthroughs and innovation, and advocating for policies that create transformative changes in kidney medicine throughout the world.

learn more

Contact ASN

1401 H St, NW, Ste 900, Washington, DC 20005


The Latest on Twitter

Kidney Week

Abstract: TH-PO914

Hyperoside Diminishes Tubulointerstitial Fibrosis in Obstructive Nephropathy via Targeting Pericyte-Myofibroblast Transition

Session Information

Category: CKD (Non-Dialysis)

  • 1903 CKD (Non-Dialysis): Mechanisms


  • Wan, Yigang, Nanjing Drum Tower Hospital, The Affiliated Hospital of Nanjing University Medical School, Nanjing, Jiangsu, China
  • Wu, Wei, Nanjing Drum Tower Hospital, The Affiliated Hospital of Nanjing University Medical School, Nanjing, Jiangsu, China

Pericyte-myofibroblast transition (PMT) plays an important role during the progression of tubulointerstitial fibrosis (TIF) in chronic kidney disease (CKD). Blocking PMT has been recognized as a potential target for anti-fibrotic therapy. In China, hyperoside (HYP), a bioactive component of Abelmoschus manihot, has been frequently used to treat TIF in CKD patients. However, the therapeutic mechanisms in vivo of the dose-effects of HYP on TIF by targeting PMT and its signaling activation remained unclear.


Twenty-five rats were divided into 5 groups, the sham, the vehicle, the high dose of HYP, the low dose of HYP and the imatinib groups. The different doses of HYP, imatinib and distilled water were administrated with intraperitoneal injections or oral for 2 weeks before and after the induction of TIF by unilateral ureteral obstruction (UUO), respectively. Rat's general status, 24 h urinary protein, urinary N-acetyl-beta-D-glucosaminidase, blood biochemical parameters, tubulointerstitial morphological changes, the markers of PMT such as platelet-derived growth factor receptor (PDGFR)β, α-smooth muscle actin (αSMA) and vimentin, as well as the key signaling molecular expressions in PDGFR pathway and vascular endothelial growth factor receptor (VEGFR) pathway in the kidney were observed, respectively.


TIF was induced in the obstructed kidneys of the UUO model rats. PMT was triggered, marked by the increased expressions of PMT markers in peritubular pericytes. In addition, TIF was aggravated by PMT and could be significantly improved by the high dose of HYP and imatinib in vivo, reflected by inhibiting PMT markers' expressions in peritubular pericytes and attenuating ECM accumulation and collagen deposition in renal interstitium. HYP and imatinib could block PMT through inhibiting PDGFR and VEGFR signalings activation. Furthermore, the effects of HYP at the high dose were partially superior to those of imatinib.


In this study, we clarified that the high dose of HYP, superior to imatinib, can attenuate TIF through blocking PMT and inhibiting the key signaling molecular expressions in PDGFR and VEGFR pathways. These findings may partly explain the therapeutic mechanisms of HYP in treating CKD, and further suggest that targeting PMT and its signaling activation may provide new strategies for TIF treatment in CKD.


  • Veterans Affairs Support