Kaempferol protects HIT-T15 pancreatic beta cells from 2-deoxy-D-ribose-induced oxidative damage

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 specie...

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Published in:Phytotherapy research 2010-03, Vol.24 (3), p.419-423
Main Authors: Lee, Yun Jung, Suh, Kwang Sik, Choi, Moon Chan, Chon, Suk, Oh, Seungjoon, Woo, Jeong-Taek, Kim, Sung-Woon, Kim, Jin-Woo, Kim, Young Seol
Format: Article
Language:English
Subjects:
2-deoxy-D-ribose
Antioxidants - pharmacology
Apoptosis
Biological and medical sciences
Cell Line
Cell Survival
Deoxyribose
diabetes mellitus
diabetes mellitus, Type 2
General pharmacology
Humans
Insulin-Secreting Cells - drug effects
Kaempferols - pharmacology
Lipid Peroxidation
Medical sciences
oxidative stress
Oxidative Stress - drug effects
Pharmacognosy. Homeopathy. Health food
Pharmacology. Drug treatments
Reactive Oxygen Species - metabolism
Type 2
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Summary: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 µM) 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. Copyright © 2009 John Wiley & Sons, Ltd.
ISSN:0951-418X
1099-1573
DOI:10.1002/ptr.2983