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Kaempferol protects HIT‐T15 pancreatic beta cells from 2‐deoxy‐D‐ribose‐induced oxidative damage
Author(s) -
Lee Yun Jung,
Suh Kwang Sik,
Choi Moon Chan,
Chon Suk,
Oh Seungjoon,
Woo JeongTaek,
Kim SungWoon,
Kim JinWoo,
Kim Young Seol
Publication year - 2010
Publication title -
phytotherapy research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.019
H-Index - 129
eISSN - 1099-1573
pISSN - 0951-418X
DOI - 10.1002/ptr.2983
Subject(s) - reactive oxygen species , lipid peroxidation , oxidative stress , chemistry , pharmacology , apoptosis , kaempferol , biochemistry , intracellular , antioxidant , biology , flavonoid
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.