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2011 | 58 | 1 | 45-50
Article title

Effects of olive leaf polyphenols against H2O2 toxicity in insulin secreting β-cells

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Abstracts
EN
In pancreatic β-cells, although H2O2 is a metabolic signal for glucose stimulated insulin secretion, it may induce injury in the presence of increased oxidative stress (OS) as in the case of diabetic chronic hyperglycemia. Olea europea L. (olive) leaves contain polyphenolic compounds that may protect insulin-secreting cells against OS. The major polyphenolic compound in ethanolic olive leaf extract (OLE) is oleuropein (about 20 %), thus we compared the effects of OLE with the effects of standard oleuropein on INS-1 cells. The cells were incubated with increasing concentrations of OLE or oleuropein for 24 h followed by exposure to H2O2 (0.035 mM) for 45 min. H2O2 alone resulted in a significantly decreased viability (MTT assay), depressed glucose-stimulated insulin secretion, increased apoptotic and necrotic cell death (AO/EB staining), inhibited glutathione peroxidase activity (GPx) and stimulated catalase activity that were associated with increased intracellular generation of reactive oxygen species (ROS) (fluorescence DCF). OLE and oleuropein partly improved the viability, attenuated necrotic and apoptotic death, inhibited the ROS generation and improved insulin secretion in H2O2-exposed cells. The effects of oleuropein on insulin secretion were more pronounced than those of OLE, while OLE exerted a stronger anti-cytotoxic effect than oleuropein. Unlike OLE, oleuropein had no significant preserving effect on GPx; however, both compounds stimulated the activity of catalase in H2O2-exposed cells. These findings indicate different modulatory roles of polyphenolic constituents of olive leaves on redox homeostasis that may have a role in the maintenance of β-cell physiology against OS.
Publisher

Year
Volume
58
Issue
1
Pages
45-50
Physical description
Dates
published
2011
received
2010-07-08
revised
2010-11-03
accepted
2010-12-18
(unknown)
2011-03-07
Contributors
  • Gazi University, Faculty of Medicine, Department of Medical Biochemistry, Ankara, Turkey
author
  • Institute of Experimental Pharmacology and Toxicology, Slovak Academy of Sciences, Bratislava, Slovak Republic
author
  • Institute of Experimental Pharmacology and Toxicology, Slovak Academy of Sciences, Bratislava, Slovak Republic
author
  • Ankara University, Faculty of Pharmacy, Department of Pharmacognosy, Ankara, Turkey
  • Geneva University, Faculty of Medicine, Department of Cell Physiology and Metabolism, Geneva, Switzerland
author
  • Gazi University, Faculty of Medicine, Department of Medical Pharmacology, Ankara, Turkey.
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Document Type
Publication order reference
Identifiers
YADDA identifier
bwmeta1.element.bwnjournal-article-abpv58i1p45kz
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