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Published on: January 23, 2018
Kaempferol protects HIT-T15 pancreatic beta cells from 2-deoxy-D-ribose-induced oxidative damage
Yun Jung Lee1, Kwang Sik Suh, Moon Chan Choi
1Department of Endocrinology and Metabolism, Kyung Hee University, School of Medicine, 1 Hoigi-Dong, Dongdaemoon-Gu, Seoul 130-702, Korea.
Abstract:
During the progression of Type 2 diabetes, glucose toxicity is likely to contribute importantly to progressive beta cell failure. Oxidative stress is an important aspect of glucose toxicity in pancreatic beta cells, and reducing sugars, such as 2-deoxy-D-ribose (dRib), produce reactive oxygen species. Furthermore, many of the biological properties of flavonoids are likely to be related to their antioxidant and free-radical scavenging abilities. Accordingly, in the present study, we investigated whether kaempferol (a flavonol) protects beta cells from dRib-induced oxidative damage. HIT-T15 cells were cultured with various concentrations of dRib for 24h. Cell survivals, amounts of reactive oxygen species (ROS) generated, apoptosis, and lipid peroxidation were measured. dRib was found to dose-dependently reduce cell survival and to markedly increase intracellular ROS levels, apoptosis, and lipid peroxidation. However, kaempferol (10 microM) suppressed dRib (20 mM) induced intracellular ROS, apoptosis, and lipid peroxidation. So, we demonstrate that kaempferol reduces dRib-mediated beta cell damage interfering with ROS metabolism and protective effects against lipid peroxidation. Our findings indicate that kaempferol protects HIT-T15 cells from dRib-induced associated oxidative damage.
Insights
Kaempferol, a flavonoid, protects pancreatic beta cells from damage caused by 2-deoxy-D-ribose (dRib), a sugar linked to Type 2 diabetes progression. This compound reduces oxidative stress and apoptosis, offering a potential therapeutic strategy.
Area of Science:
- Biochemistry
- Cell Biology
- Endocrinology
Background:
- Type 2 diabetes progression involves beta cell failure, exacerbated by glucose toxicity.
- Oxidative stress in pancreatic beta cells is a key component of glucose toxicity.
- Reducing sugars like 2-deoxy-D-ribose (dRib) generate reactive oxygen species (ROS), contributing to cellular damage.
Purpose of the Study:
- To investigate the protective effects of kaempferol, a flavonol, against 2-deoxy-D-ribose (dRib)-induced oxidative damage in pancreatic beta cells.
- To determine if kaempferol can mitigate dRib-induced increases in reactive oxygen species (ROS), apoptosis, and lipid peroxidation.
Main Methods:
- HIT-T15 cells were exposed to various concentrations of dRib.
- Kaempferol (10 microM) was administered to assess its protective effects.
- Measurements included cell survival, intracellular ROS levels, apoptosis, and lipid peroxidation.
Main Results:
- dRib significantly reduced cell survival in a dose-dependent manner.
- dRib markedly increased intracellular ROS levels, apoptosis, and lipid peroxidation.
- Kaempferol treatment suppressed dRib-induced ROS generation, apoptosis, and lipid peroxidation.
Conclusions:
- Kaempferol demonstrates protective effects against dRib-mediated beta cell damage.
- Kaempferol mitigates dRib-induced oxidative stress by interfering with ROS metabolism.
- The findings suggest kaempferol's potential role in protecting pancreatic beta cells from diabetes-associated oxidative damage.
