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Ginsenoside Rb1 ameliorates CKD-associated vascular calcification by inhibiting the Wnt/β-catenin pathway

Peng Zhou1, Xinyu Zhang1, Mengqi Guo1

  • 1The Key Laboratory of Cardiovascular Remodeling and Function Research, Chinese Ministry of Education, Chinese National Health Commission and Chinese Academy of Medical Sciences, The State and Shandong Province Joint Key Laboratory of Translational Cardiovascular Medicine, Department of Cardiology, Qilu Hospital of Shandong University, Jinan, China.

Journal of Cellular and Molecular Medicine
|August 20, 2019
PubMed

Insights

Ginsenoside Rb1 (Rb1) reduces vascular calcification in chronic kidney disease models by activating PPAR-γ and inhibiting the Wnt/β-catenin pathway. This study reveals Rb1

Area of Science:

  • Cardiovascular Biology
  • Nephrology
  • Pharmacology

Background:

  • Vascular calcification (VC) is a major contributor to cardiovascular disease morbidity and mortality.
  • Chronic kidney disease (CKD) is frequently associated with VC, highlighting the need for therapeutic targets.
  • The cardiovascular protective effects of Ginsenoside Rb1 (Rb1) are known, but its role in VC remains unexplored.

Purpose of the Study:

  • To investigate the therapeutic potential of Ginsenoside Rb1 (Rb1) in mitigating vascular calcification (VC).
  • To elucidate the underlying molecular mechanisms of Rb1's action in VC, particularly its interaction with the Wnt/β-catenin pathway.

Main Methods:

  • Established in vivo (CKD-associated VC rat model) and in vitro (β-glycerophosphate-induced VSMC calcification) models.
  • Administered Rb1 and assessed its effects on calcium deposition and VSMC osteogenic transdifferentiation.
  • Utilized confocal microscopy to observe β-catenin nuclear translocation and employed pathway modulators (SKL2001, GW9662) to confirm mechanisms.

Main Results:

  • Rb1 significantly ameliorated calcium deposition and prevented VSMC osteogenic transdifferentiation in both experimental models.
  • Rb1 activated peroxisome proliferator-activated receptor-γ (PPAR-γ), which subsequently inhibited the Wnt/β-catenin pathway by preventing β-catenin nuclear translocation.
  • Pharmacological inhibition of Wnt/β-catenin (SKL2001) diminished Rb1's protective effects, while PPAR-γ antagonism (GW9662) reversed Rb1's inhibition of β-catenin.

Conclusions:

  • Ginsenoside Rb1 (Rb1) demonstrates significant anticalcific properties in the context of chronic kidney disease-associated vascular calcification.
  • Rb1 exerts its protective effects by activating PPAR-γ, leading to the inhibition of the Wnt/β-catenin signaling pathway.
  • The findings suggest that the PPAR-γ/Wnt/β-catenin axis is a key mediator of Rb1's therapeutic action, offering new avenues for VC treatment.

Keywords:
PPAR-γWnt/β-cateninginsenoside Rb1vascular calcification

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