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Isolated Pancreatic Islet Treatment and Apoptosis Measurement
Published on: May 2, 2025
Mulberry fruit extract protects pancreatic β-cells against hydrogen peroxide-induced apoptosis via antioxidative
Jong Seok Lee1, Young Rae Kim2, Jun Myoung Park3
1Department of Bioengineering and Technology, Kangwon National University, Chuncheon 200701, Korea. jongseoklee78@gmail.com.
Abstract:
Among the many environmental stresses, excessive production of reactive oxygen species (ROS) and the ensuring oxidative stress are known to cause significant cellular damage. This has clinical implications in the onset of type 1 diabetes, which is triggered by the destruction of pancreatic β-cells and is associated with oxidative stress. In this study, we investigated the protective and antioxidative effects of mulberry extract (ME) in insulin-producing pancreatic β-cells. We found that ME protects pancreatic β-cells against hydrogen peroxide (H2O2)-induced oxidative stress and the associated apoptotic cell death. ME treatment significantly reduced the levels of H2O2-induced 2-diphenyl-1-picrylhydrazyl (DPPH) radicals, and lipid peroxidation and intracellular ROS accumulation. In addition, ME inhibited DNA condensation and/or fragmentation induced by H2O2. These results suggest that ME protects pancreatic β-cells against hydrogen peroxide-induced oxidative stress.
Insights
Mulberry extract (ME) protects pancreatic beta-cells from oxidative stress and cell death. ME reduces reactive oxygen species (ROS) and DNA damage, offering a potential therapeutic approach for type 1 diabetes.
Area of Science:
- Biochemistry
- Cell Biology
- Pharmacology
Background:
- Oxidative stress from excessive reactive oxygen species (ROS) causes cellular damage.
- Type 1 diabetes involves pancreatic beta-cell destruction linked to oxidative stress.
Purpose of the Study:
- To investigate the protective and antioxidative effects of mulberry extract (ME) on insulin-producing pancreatic beta-cells.
Main Methods:
- Cells were exposed to hydrogen peroxide (H2O2) to induce oxidative stress.
- ME treatment effects on DPPH radicals, lipid peroxidation, intracellular ROS, and DNA integrity were assessed.
Main Results:
- ME significantly reduced H2O2-induced DPPH radicals, lipid peroxidation, and intracellular ROS.
- ME inhibited H2O2-induced DNA condensation and fragmentation.
- ME demonstrated protective effects against H2O2-induced apoptotic cell death.
Conclusions:
- Mulberry extract exhibits significant protective and antioxidative properties in pancreatic beta-cells.
- ME mitigates oxidative stress and prevents apoptosis, suggesting therapeutic potential for type 1 diabetes.
