Publication: Curcumin I protects the dopaminergic cell line SH-SY5Y from 6-hydroxydopamine-induced neurotoxicity through attenuation of p53-mediated apoptosis
Issued Date
2011-02-11
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ISSN
03043940
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2-s2.0-78751575381
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Mahidol University
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SCOPUS
Bibliographic Citation
Neuroscience Letters. Vol.489, No.3 (2011), 192-196
Suggested Citation
Yamaratee Jaisin, Anusorn Thampithak, Benjawan Meesarapee, Piyanee Ratanachamnong, Apichart Suksamrarn, Laddawal Phivthong-ngam, Noppawan Phumala-Morales, Sukumal Chongthammakun, Piyarat Govitrapong, Yupin Sanvarinda Curcumin I protects the dopaminergic cell line SH-SY5Y from 6-hydroxydopamine-induced neurotoxicity through attenuation of p53-mediated apoptosis. Neuroscience Letters. Vol.489, No.3 (2011), 192-196. doi:10.1016/j.neulet.2010.12.014 Retrieved from: https://repository.li.mahidol.ac.th/handle/20.500.14594/12790
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Title
Curcumin I protects the dopaminergic cell line SH-SY5Y from 6-hydroxydopamine-induced neurotoxicity through attenuation of p53-mediated apoptosis
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Abstract
Oxidative stress (OS) plays a pivotal role in the pathogenesis of Parkinson's disease (PD). 6-Hydroxydopamine (6-OHDA) is a neurotoxin used to induce oxidative cell death of dopaminergic neurons in experimental models of PD. Curcumin I, or diferuloylmethane is a pure compound isolated from Curcuma longa Linn. that has been reported to have neuroprotective properties. The precise mechanism, however, remains unclear. This study aims to elucidate the mechanisms by which curcumin I exerts its effects, using 6-OHDA-induced neurotoxicity in the human dopaminergic cell line SH-SY5Y. In our experiments, pretreatment with curcumin I improved cell viability, and significantly reduced reactive oxygen species (ROS). Further investigations revealed a reduction of p53 phosphorylation and decrease of the Bax/Bcl-2 ratio, as measured by mRNA expression and protein level. Taken together, these findings indicate that curcumin I protects dopaminergic neurons from 6-OHDA-induced toxicity via the reduction of ROS production, and subsequent attenuation of p53 phosphorylation and reduction of the Bax/Bcl-2 ratio. © 2010 Elsevier Ireland Ltd.