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Mechanism of Kemeng Fang's Inhibition of Podocyte Apoptosis in Rats with Membranous Nephropathy through the PI3K/AKT Signaling Pathway
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Mechanism of Kemeng Fang's Inhibition of Podocyte Apoptosis in Rats with Membranous Nephropathy through the PI3K/AKT Signaling Pathway

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Gypenoside Inhibits Endothelial Cell Apoptosis in Atherosclerosis by Modulating Mitochondria through PI3K/Akt/Bad

Nan Song1,2, Lianqun Jia1,2, Huimin Cao1,2

  • 1Key Laboratory of Ministry of Education for TCM Viscera-State Theory and Applications, Liaoning University of Traditional Chinese Medicine, Shenyang 110847, China.

Biomed Research International
|July 21, 2020
PubMed

Insights

Gypenoside, a natural compound, reduces atherosclerosis by protecting endothelial cells from apoptosis. It modulates mitochondrial function and the PI3K/Akt/Bad pathway, offering therapeutic potential for this common disease.

Area of Science:

  • Cardiovascular Biology
  • Molecular Medicine
  • Pharmacology

Background:

  • Atherosclerosis is a leading global cause of mortality.
  • Endothelial cell apoptosis contributes significantly to atherosclerosis progression by impairing lipid homeostasis, inflammation, and immune regulation.
  • Endothelial injury disrupts barrier function, promoting lipid deposition and atherogenesis.

Purpose of the Study:

  • To investigate the potential of gypenoside, a natural product derived from Chinese medicine, in preventing and treating atherosclerosis.
  • To elucidate the molecular mechanisms underlying gypenoside's effects on endothelial cell apoptosis and mitochondrial function in atherosclerosis.

Main Methods:

  • Administration of gypenoside to a mouse model of atherosclerosis.
  • Assessment of serum lipid levels, atherosclerotic plaque formation, and aortic intima thickening.
  • Analysis of the PI3K/Akt/Bad signaling pathway and apoptosis-related protein expression in the aorta.
  • Evaluation of mitochondrial fission and fusion proteins, and mitochondrial energy-related proteins.

Main Results:

  • Gypenoside treatment decreased serum lipid levels, alleviated atherosclerotic plaque formation, and reduced aortic intima thickening.
  • Gypenoside activated the PI3K/Akt/Bad signaling pathway, modulating apoptosis-related protein expression.
  • Gypenoside downregulated mitochondrial fission and fusion proteins, and mitochondrial energy-related proteins in mouse aortas.

Conclusions:

  • Gypenoside exhibits a protective effect against atherosclerosis by mitigating endothelial cell apoptosis.
  • Gypenoside's therapeutic potential lies in its ability to modulate mitochondrial function via the PI3K/Akt/Bad pathway.
  • Gypenoside represents a promising natural therapeutic agent for atherosclerosis associated with endothelial apoptosis.

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