Volume 7 Supplement 1

Proceedings of the 2011 International Conference on Molecular Neurodegeneration

Open Access

Protective effect of uric acid against 6-OHDA-induced injury in SH-SY5Y cells

Molecular Neurodegeneration20127(Suppl 1):S12

https://doi.org/10.1186/1750-1326-7-S1-S12

Published: 7 February 2012

Objective

To investigate the effect of uric acid (UA) on 6-hydroxydopamine (6-OHDA) -induced injury in SH-SY5Y cells.

Methods

The cell viability was measured by the MTT reduction assay. The cell apoptosis was assessed by Hoechst 33342 staining with fluorescence microscopy. The phophorylation of Akt and GSK-3β(ser9) was determined by Western blot analysis.

Results

Treatment with 6-OHDA at 50µM for 12 h significantly decreased the viability of SH-SY5Y cells. Pretreatment with UA (200-400µM, 0.5h) prior to 6-OHDA treatment markedly increased the cell viability of SH-SY5Y cells, as compared to that of 6-OHDA-treated group. The beneficial effects of UA against 6-OHDA-induced apoptosis were also confirmed by Hoechst 33342 staining assay. Moreover, 6-OHDA decreased the Akt activity and increased the GSK-3β activity, which could be blocked by UA (200-400µM) pretreatment.

Conclusions

These data suggest that 6-OHDA-induced cell injury was attenuated by UA. The underlying mechanisms may involve the up-regulation of Akt and the reduction of GSK-3β activity.

Declarations

Acknowledgements

Contract grant sponsor: The work was supported by the Suzhou Foundation for Development of Science, Technology (200815404), Jiangsu Ordinary University Science Research Project (08KJB320012) and Natural Science Foundation of Jiangsu Province, China (BK2010229).

Authors’ Affiliations

(1)
The Department of Neurology, Second Affiliated Hospital of Soochow University
(2)
The Institute of Neuroscience of Soochow University

Copyright

© Huang et al; licensee BioMed Central Ltd. 2012

This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

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