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  11. Dihydroquercetin Improves Experimental Acute Liver Failure By Targeting Ferroptosis And Mitochondria-mediated Apoptosis Through The Sirt1/p53 Axis

Dihydroquercetin improves experimental acute liver failure by targeting ferroptosis and mitochondria-mediated apoptosis through the SIRT1/p53 axis

Yuqiao Zeng1, Yiyu He2, Li Wang1

  • 1Shandong Second Medical University, Weifang, Shandong 261053, China.

Phytomedicine : International Journal of Phytotherapy and Phytopharmacology
|March 29, 2024

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View abstract on PubMed

Summary
This summary is machine-generated.

Dihydroquercetin (DHQ) protects against acute liver failure (ALF) by inhibiting ferroptosis and mitochondria-mediated apoptosis. This novel therapy targets the SIRT1/p53 pathway, offering potential for ALF treatment.

Area of Science:

  • Biochemistry
  • Cell Biology
  • Pharmacology

Background:

  • Acute liver failure (ALF) involves both ferroptosis and mitochondria-mediated apoptosis.
  • Ferroptosis-induced reactive oxygen species (ROS) can promote mitochondrial apoptosis.
  • Dihydroquercetin (DHQ) demonstrates protective effects against liver injury.

Purpose of the Study:

  • To investigate the protective effects of DHQ on ALF.
  • To elucidate the underlying molecular mechanisms of DHQ's action in ALF.

Main Methods:

  • Established mouse (LPS/D-Gal) and cell (TNF-α/D-Gal) models of ALF.
  • Assessed ROS, lipid peroxidation, mitochondrial membrane potential, and apoptosis.
  • Utilized gene expression (QRT-PCR) and protein analysis (Western blot), including SIRT1 and p53 modulation.
Keywords:
Acute liver failureDihydroquercetinFerroptosisMitochondria-mediated apoptosis

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Main Results:

  • DHQ treatment ameliorated ALF, reduced ROS and lipid peroxidation, and preserved mitochondrial function.
  • DHQ inhibited ferroptosis and mitochondria-mediated apoptosis by upregulating SIRT1 and enhancing p53 deacetylation.
  • SIRT1 knockdown or p53 activation reversed DHQ's protective effects, while SLC7A11 overexpression or Apaf-1 knockdown partially attenuated apoptosis.

Conclusions:

  • DHQ alleviates ALF by inhibiting ferroptosis and mitochondria-mediated apoptosis via the SIRT1/p53 pathway.
  • DHQ presents potential as a novel therapeutic agent for acute liver failure.
SIRT1/p53 axis