| Abstract No.: | A-C1083 |
| Country: | Canada |
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| Title: | QUERCETIN, A NATURAL POLYPHENOL, REDUCES APOPTOTIC DEATH IN NEURONAL PC12 CELLS. |
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| Authors/Affiliations: | 1 Julie Bournival*; 1 Maria-Grazia Martinoli;
1 UQTR, Trois-Rivières, QC, Canada
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| Content: | Parkinson’s disease (PD) is a common neurodegenerative disorder with the clinical features, including slowness of movement, stiffness, tremor and postural instability. Although the etiology of PD is still not completely understood, many factors are speculated to operate in the mechanism of cell death of nigrostriatal dopaminergic (DAergic) neurons. Reactive oxygen species (ROS) produced by oxidative stress may participate to the apoptotic death of DAergic neurons distinctive of PD.
Quercetin, a natural polyphenol found mainly in green tea, is well known for its antioxidant propertie on a DAergic neuronal model (neuronal PC12 cells), as we already demonstrated. The aim of this study is to explore the effect of quercetin against MPP+-induced apoptosis and its molecular mechanisms, in PC12 cells. Apoptotic nuclei were stained by TUNEL assay and the presence of cleaved caspase-3 was detected by immunofluorescence. Our findings indicate that MPP+ significantly induced apoptosis of PC12 cells (45%) and a quercetin pre-treatment could reduce apoptotic neuronal PC12 death to 23%. We also studied the effect of quercetin on the expression of Bax (a pro-apototic gene) and Bcl-2 (an anti-apoptotic gene) by RT-PCR. Quercetin administered 3h prior to MPP+ reduced significantly Bax mRNA levels but did not increased significantly Bcl-2 mRNA levels. Using immunoblot analysis, we also evaluated the release of cytochrome C. A quercetin pre-treatment led to the decrease of cytosolic cytochrome C protein expression. Our results demonstrate that quercetin diminish apoptotic neuronal cell death and suggest that this natural polyphenol act on the expression of pro-apoptotic genes, such as Bax. These findings support the role of natural compounds as a possible preventive and/or complementary therapy for several human neurodegenerative diseases caused by oxidative stress, such as PD.
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