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Related Experiment Video

Updated: Jun 16, 2025

Induction of Atherosclerotic Plaques Through Activation of Mineralocorticoid Receptors in Apolipoprotein E-deficient Mice
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β-sitosterol alleviates atherosclerosis by regulating catalase.

Shuntao Jiang1, Kui Gao2, Furong Zhang3

  • 1Department of Cardiovascular Medicine, Affiliated Hospital of Zunyi Medical University, No. 149, Dalian Road, Huichuan District, Zunyi, 563000, Guizhou, China.

Heliyon
|August 21, 2024
PubMed
Summary

Beta-sitosterol from Gegen (Puerariae Lobatae Radix) effectively combats atherosclerosis by inhibiting plaque formation and lipid deposition. It works by activating catalase and silencing the PI3K/Akt/mTOR pathway, offering a potential therapeutic strategy.

Keywords:
AtherosclerosisLipid depositionPuerariae lobatae radixVSMCs phenotypic transformationβ-sitosterol

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Area of Science:

  • Pharmacology
  • Biochemistry
  • Cardiovascular Research

Background:

  • Atherosclerosis is a chronic inflammatory disease characterized by plaque buildup in arteries.
  • Gegen (Puerariae Lobatae Radix) is a traditional Chinese medicine with potential cardiovascular benefits.
  • Identifying active components and mechanisms is crucial for therapeutic development.

Purpose of the Study:

  • To identify the primary active component of Gegen responsible for anti-atherosclerotic effects.
  • To elucidate the mechanism of action of this component in preventing and treating atherosclerosis.

Main Methods:

  • Bioinformatics analysis to predict active compounds.
  • In vivo studies assessing plaque formation, platelet activation, and lipid profiles.
  • In vitro experiments evaluating lipid deposition and vascular smooth muscle cell (VSMC) behavior.
  • Gene knockdown and pathway inhibition experiments (catalase, PI3K/Akt/mTOR).

Main Results:

  • Beta-sitosterol identified as a key anti-atherosclerotic component of Gegen.
  • In vivo: Beta-sitosterol reduced plaque formation, platelet activation, serum total cholesterol, and triglycerides.
  • In vitro: Beta-sitosterol inhibited VSMC lipid deposition and phenotypic transformation.
  • Catalase knockdown exacerbated lipid deposition and VSMC changes, activating the PI3K/Akt/mTOR pathway.
  • mTOR inhibition reversed the effects of catalase knockdown.

Conclusions:

  • Beta-sitosterol alleviates atherosclerosis by inhibiting VSMC lipid deposition and phenotypic transformation.
  • The mechanism involves activating catalase and suppressing the PI3K/Akt/mTOR signaling pathway.
  • Beta-sitosterol represents a promising therapeutic agent for atherosclerosis.