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Abstract: TH-PO549

Hirudin Alleviates Renal Fibrosis by Regulating PDGFB Pathway Based on Bioinformatics

Session Information

  • Pathology and Lab Medicine
    November 03, 2022 | Location: Exhibit Hall, Orange County Convention Center‚ West Building
    Abstract Time: 10:00 AM - 12:00 PM

Category: Pathology and Lab Medicine

  • 1700 Pathology and Lab Medicine


  • Li, Ying, Chongqing Hospital of Traditional Chinese Medicine, Chongqing, China
  • Xiong, Weijian, Chongqing Hospital of Traditional Chinese Medicine, Chongqing, China

RIF is the final pathological manifestation of most patients with CKD and a precursor of end-stage renal disease, In recent years, many reports have confirmed the therapeutic effect of hirudin in renal disease.Our study was committed to revealing the hirudin’s reduction to renal fibrosis(RF) as well as the molecular mechanism.


To begin with, we commenced both the identification and the determination to the hirudin targeted proteins and its down-stream signaling pathways with the methods of bioinformatics, molecular docking and coprecipitation. After that, we validated hirudin’s interaction with PDGFB with the assays of molecular docking and immunoprecipitation.


With the help of CTD database, 10 target proteins of hirudin were obtained, and N proteins were screened by mass spectrometry analysis.5 proteins were screened out and 5 flag-target overexpressed plasmid vectors were constructed respectively, which were verified by immunoprecipitation in NRK-52E cells. We found that only PDGF-BB is capable of binding to hirudin. Subsequently, we confirmed that hirudin inhibits the EMT caused by PI3K-AKT by reducing the phosphorylation of PDGFRβ in vitro.


Hirudin reduces the phosphorylation level of PDGFRβ by binding to PDGF-BB.


  • Government Support – Non-U.S.