NDLI: Beneficial effect of the bioflavonoid quercetin on cholecystokinin-induced mitochondrial dysfunction in isolated rat pancreatic acinar cells.

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Beneficial effect of the bioflavonoid quercetin on cholecystokinin-induced mitochondrial dysfunction in isolated rat pancreatic acinar cells.

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Year: 2014 Volume: 92 Issue: 2

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Beneficial effect of the bioflavonoid quercetin on cholecystokinin-induced mitochondrial dysfunction in isolated rat pancreatic acinar cells.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Weber, Heike Jonas, Ludwig Wakileh, Michael Krüger, Burkhard
Description	Country affiliation: Germany Author Affiliation: Weber H ( a Institute of Clinical Chemistry and Laboratory Medicine, University of Rostock, Ernst-Heydemann-Straße 6, 18057 Rostock, Germany.)
Abstract	The pathogenesis of acute pancreatitis (AP) is still poorly understood. Thus, a reliable pharmacological therapy is currently lacking. In recent years, an impairment of the energy metabolism of pancreatic acinar cells, caused by Ca(2+)-mediated depolarization of the inner mitochondrial membrane and a decreased ATP supply, has been implicated as an important pathological event. In this study, we investigated whether quercetin exerts protection against mitochondrial dysfunction. Following treatment with or without quercetin, rat pancreatic acinar cells were stimulated with supramaximal cholecystokinin-8 (CCK). CCK caused a decrease in the mitochondrial membrane potential (MMP) and ATP concentration, whereas the mitochondrial dehydrogenase activity was significantly increased. Quercetin treatment before CCK application exerted no protection on MMP but increased ATP to a normal level, leading to a continuous decrease in the dehydrogenase activity. The protective effect of quercetin on mitochondrial function was accompanied by a reduction in CCK-induced changes to the cell membrane. Concerning the molecular mechanism underlying the protective effect of quercetin, an increased AMP/ATP ratio suggests that the AMP-activated protein kinase system may be activated. In addition, quercetin strongly inhibited CCK-induced trypsin activity. The results indicate that the use of quercetin may be a therapeutic strategy for reducing the severity of AP.
File Format	HTM / HTML
ISSN	00084212
e-ISSN	12057541
Journal	Canadian Journal of Physiology and Pharmacology
Issue Number	3
Volume Number	92
Language	English
Publisher	Canadian Science Publishing
Publisher Date	2014-03-01
Publisher Place	Canada
Access Restriction	Open
Subject Keyword	Discipline Physiology Discipline Pharmacology Acinar Cells Drug Effects Antioxidants Pharmacology Cholecystokinin Mitochondria Pancreas Peptide Fragments Quercetin Cytology Metabolism Adenosine Triphosphate Animals Cell Survival Cells, Cultured Free Radical Scavengers Membrane Potential, Mitochondrial Physiology Oxidoreductases Pancreatic Elastase Pancreatitis, Acute Necrotizing Drug Therapy Trypsin
Content Type	Text
Resource Type	Article
Subject	Physiology Physiology (medical) Pharmacology

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