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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.
Summary
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.
- 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.
