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Updated: Jun 19, 2026
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Identification of Intracellular Signaling Events Induced in Viable Cells by Interaction with Neighboring Cells Undergoing Apoptotic Cell Death
Published on: December 27, 2016
Apoptosis in HepG2 cells exposed to high glucose
Karthikeyan Chandrasekaran1, Kavitha Swaminathan, Suvro Chatterjee
1Life Science Division, AU-KBC Research Centre, MIT Campus of Anna University, Chromepet, Chennai 600 044, India.
Summary
High glucose levels trigger cell death in liver cells by increasing oxidative stress. Antioxidant treatment reversed these harmful effects, confirming oxidative stress as a key mechanism in hyperglycemia-induced apoptosis.
Area of Science:
- Cell Biology
- Biochemistry
- Toxicology
Background:
- Hyperglycemia, a hallmark of diabetes, disrupts cellular functions.
- Understanding glucose toxicity in liver cells is crucial for diabetes management.
Purpose of the Study:
- To investigate the toxic effects of high glucose concentrations on human hepatoma HepG2 cells.
- To elucidate the role of oxidative stress in glucose-induced apoptosis.
Main Methods:
- HepG2 cells were incubated with 50mM glucose for 72 hours.
- Assessed cell morphology, viability, apoptosis markers (caspase-3, Annexin V), and oxidative stress indicators (ROS, lipid peroxidation, protein carbonyls, 3-nitrotyrosine).
- Evaluated the protective effect of N-Acetyl cysteine (NAC).
Main Results:
- High glucose induced significant morphological changes and decreased cell viability in HepG2 cells.
- Apoptosis was confirmed by increased caspase-3 activity and Annexin V staining.
- Elevated oxidative stress markers (ROS, lipid peroxidation, protein carbonyls, 3-nitrotyrosine) were observed.
- Intracellular glutathione levels increased, and NAC treatment reversed glucose-induced toxicity and oxidative stress.
Conclusions:
- High glucose induces apoptosis in HepG2 liver cells primarily through increased oxidative stress.
- N-Acetyl cysteine demonstrates a protective effect, validating the role of oxidative stress in this process.
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