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 X

Kidney Week

Please note that you are viewing an archived section from 2022 and some content may be unavailable. To unlock all content for 2022, please visit the archives.

Abstract: FR-PO998

A Molecular Mechanism Study to Reveal Hirudin Downregulation to PI3K/AKT Signaling Pathway With PDGFB in Renal Fibrosis Treatment

Session Information

  • CKD: Pathobiology - I
    November 04, 2022 | Location: Exhibit Hall, Orange County Convention Center‚ West Building
    Abstract Time: 10:00 AM - 12:00 PM

Category: CKD (Non-Dialysis)

  • 2203 CKD (Non-Dialysis): Mechanisms


  • Li, Ying, Chongqing Traditional Chinese Medicine Hospital, Chongqing, Chongqing, China
  • Tu, Haitao, The First Affiliated Hospital of Guangzhou University of Chinese Medicine, Guangzhou, Guangdong, China

Chronic kidney disease, also known as CKD, is a prevalent chronic disease jeopardizing public health; however, there is no an efficient therapy to prevail over this disease. Our study was committed to revealing the hirudin's regulation to chronic kidney disease as well as the molecular mechanism.


We built renal fibrosis model on animal levels, which was subsequently given with hirudin disposal, then we performed the HE and Masson to evaluate for renal fibrosis (RF) and had our detection to relevant marker proteins of RIF with western blot. Finally, we detected on the expressions of PDGFRBB, PDGFRβ and the PI3K-AKT pathway.


Our outcomes of the animal level demonstrated that the conditions of severe tubular dilatation or atrophy, interstitial fibrosis, inflammatory cell infiltration, and massive deposition of interstitial collagen in model group were withdrew after the addition of hirudin. WB results showed that the marker proteins of RF, PDGFRBB, PDGFRβ and the PI3K-AKT signal molecules were significantly reduced by addition of hirudin.


The declining in PDGFRβ phosphorylation because of the hirudin's interaction with PDGF-BB is capable of suppressing PI3K-AKT signaling pathway as well as the EMT.

Figure. 1 Alleviating ability of hirudin on the renal fibrosis of rat

Figure. 2 Detection on the expressions of the PI3K-AKT pathway


  • Government Support – Non-U.S.