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Related Experiment Video

Updated: May 10, 2026

Drug-Induced Senescence in Liver Cells Promotes M2 Macrophage Polarization: Implications for Tyrosine Kinase Inhibitor-Associated Hepatotoxicity
09:32

Drug-Induced Senescence in Liver Cells Promotes M2 Macrophage Polarization: Implications for Tyrosine Kinase Inhibitor-Associated Hepatotoxicity

Published on: October 17, 2025

Triterpenoid pristimerin induced HepG2 cells apoptosis through ROS-mediated mitochondrial dysfunction.

Yan Guo1, Wei Zhang, Yan-Yan Yan

  • 1Wuhai Municipal People's Hospital, Wuhai, Inner Mongolia, People's Republic of China.

Journal of B.U.ON. : Official Journal of the Balkan Union of Oncology
|July 3, 2013
PubMed
Summary

Related Concept Videos

Electron Transport Chain: Complex I and II01:46

Electron Transport Chain: Complex I and II

The mitochondrial electron transport chain (ETC) is the main energy generation system in the eukaryotic cells. However, mitochondria also produce cytotoxic reactive oxygen species (ROS) due to the large electron flow during oxidative phosphorylation. While Complex I is one of the primary sources of superoxide radicals, ROS production by Complex II is uncommon and may only be observed in cancer cells with mutated complexes.
ROS generation is regulated and maintained at moderate levels necessary...

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Pristimerin, a natural compound, effectively kills liver cancer cells (HepG2) by triggering programmed cell death (apoptosis). This process involves reactive oxygen species (ROS) and mitochondrial dysfunction.

Area of Science:

  • Pharmacology
  • Cell Biology
  • Biochemistry

Background:

  • Hepatocellular carcinoma (HCC) is a major global health concern.
  • Natural compounds offer potential therapeutic strategies for cancer treatment.
  • Pristimerin is a triterpenoid with known biological activities.

Purpose of the Study:

  • To investigate the anticancer effects of pristimerin on human hepatocellular carcinoma (HCC) HepG2 cells.
  • To elucidate the mechanisms underlying pristimerin-induced apoptosis and proliferation inhibition.

Main Methods:

  • Cytotoxicity assessed by MTT assay.
  • Apoptosis evaluated using Hoechst staining, Annexin V/PI, and caspase-3 activation.
  • Mitochondrial membrane potential (ΔΨm) and reactive oxygen species (ROS) measured by flow cytometry.

Related Experiment Videos

Last Updated: May 10, 2026

Drug-Induced Senescence in Liver Cells Promotes M2 Macrophage Polarization: Implications for Tyrosine Kinase Inhibitor-Associated Hepatotoxicity
09:32

Drug-Induced Senescence in Liver Cells Promotes M2 Macrophage Polarization: Implications for Tyrosine Kinase Inhibitor-Associated Hepatotoxicity

Published on: October 17, 2025

  • Protein expression analyzed via Western blot.
  • Main Results:

    • Pristimerin demonstrated potent dose-dependent cytotoxicity against HepG2 cells.
    • Apoptotic morphology, increased Annexin V-positive cells, and caspase-3 activation were observed.
    • Pristimerin induced ROS generation, mitochondrial membrane potential collapse, and cytochrome C release.
    • Changes in Bcl-2, Bax, and EGFR expression were noted, with downstream pathway inhibition.

    Conclusions:

    • Pristimerin effectively induces apoptosis in HepG2 cells.
    • Reactive oxygen species (ROS) play a critical role in pristimerin-mediated apoptosis.
    • Mitochondrial pathways are significantly involved in pristimerin's anticancer effects.