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Conference Paper: Oxyresveratrol mitigates cellular toxicity in an in-vitro and in-vivo model of Parkinson's disease

TitleOxyresveratrol mitigates cellular toxicity in an in-vitro and in-vivo model of Parkinson's disease
Authors
Issue Date2017
PublisherS Karger AG. The Journal's web site is located at http://www.karger.com/NDD
Citation
Abstracts of the 13th International Conference on Alzheimer’s & Parkinson’s Diseases, Vienna, Austria, 29 March-2 April 2017. In Neurodegenerative Diseases, 2017, v. 17 n. Suppl 1, p. 1470 How to Cite?
AbstractAims: The role of endoplasmic reticulum (ER) stress and the unfolded protein response (UPR) has been greatly demonstrated as a pathological phenomenon in Parkinson’s disease (PD). These signalling mechanisms are activated when there is an increased burden of misfolded proteins in neurons, primarily alpha synuclein, in the case of PD. In this study we aim to elucidate the effects of oxyresveratrol, a potent antioxidant, on the UPR in PD. Furthermore, the neuro-protective potential of oxyresveratrol in an in-vivo model was tested. Method: The murine dopaminergic Mes 23.5 cell line was treated with the parkinsonian mimetic 6-hydroxydopamine (6-OHDA). Effects of oxyresveratrol on the downstream effectors mediating the UPR were investigated by immunoblotting and quantitative PCR. For the in-vivo model, male Sprague-Dawley rats were injected stereotactically with 6-OHDA. Subsequently, immunohistochemistry to study midbrain pathology and behaviour tests to assess motor debilitation, were performed. Results: Oxyresveratrol reduced the expression of ATF4 and CHOP, following induction of ER stress in the Mes 23.5 cells by 6-OHDA. The activation of this branch of the UPR, downstream of PERK, propels the cell towards apoptosis. Motor dysfunction was also alleviated in the oxyresveratrol-treated rats, along with a partial preservation of dopaminergic cells in the substantia nigra pars compacta. Conclusion: This study suggests that attenuation of apoptosis driven by the UPR may be an important mechanism of action of oxyresveratrol. Moreover, a protection of motor function and cell loss seen in the in vivo model suggests that oxyresveratrol may be a useful therapeutic candidate for PD.
DescriptionC02.g. Therapeutic Targets, Mechanisms for Treatment: Anti-inflammatory, anti-oxidant - no. ADPD7-0264
Persistent Identifierhttp://hdl.handle.net/10722/248343
ISSN
2017 Impact Factor: 2.785
2015 SCImago Journal Rankings: 1.472

 

DC FieldValueLanguage
dc.contributor.authorShah, AN-
dc.contributor.authorHung, HLC-
dc.contributor.authorCheng, SSY-
dc.contributor.authorWong, MY-
dc.contributor.authorLegido-Quigley, C-
dc.contributor.authorChang, RCC-
dc.date.accessioned2017-10-18T08:41:42Z-
dc.date.available2017-10-18T08:41:42Z-
dc.date.issued2017-
dc.identifier.citationAbstracts of the 13th International Conference on Alzheimer’s & Parkinson’s Diseases, Vienna, Austria, 29 March-2 April 2017. In Neurodegenerative Diseases, 2017, v. 17 n. Suppl 1, p. 1470-
dc.identifier.issn1660-2854-
dc.identifier.urihttp://hdl.handle.net/10722/248343-
dc.descriptionC02.g. Therapeutic Targets, Mechanisms for Treatment: Anti-inflammatory, anti-oxidant - no. ADPD7-0264-
dc.description.abstractAims: The role of endoplasmic reticulum (ER) stress and the unfolded protein response (UPR) has been greatly demonstrated as a pathological phenomenon in Parkinson’s disease (PD). These signalling mechanisms are activated when there is an increased burden of misfolded proteins in neurons, primarily alpha synuclein, in the case of PD. In this study we aim to elucidate the effects of oxyresveratrol, a potent antioxidant, on the UPR in PD. Furthermore, the neuro-protective potential of oxyresveratrol in an in-vivo model was tested. Method: The murine dopaminergic Mes 23.5 cell line was treated with the parkinsonian mimetic 6-hydroxydopamine (6-OHDA). Effects of oxyresveratrol on the downstream effectors mediating the UPR were investigated by immunoblotting and quantitative PCR. For the in-vivo model, male Sprague-Dawley rats were injected stereotactically with 6-OHDA. Subsequently, immunohistochemistry to study midbrain pathology and behaviour tests to assess motor debilitation, were performed. Results: Oxyresveratrol reduced the expression of ATF4 and CHOP, following induction of ER stress in the Mes 23.5 cells by 6-OHDA. The activation of this branch of the UPR, downstream of PERK, propels the cell towards apoptosis. Motor dysfunction was also alleviated in the oxyresveratrol-treated rats, along with a partial preservation of dopaminergic cells in the substantia nigra pars compacta. Conclusion: This study suggests that attenuation of apoptosis driven by the UPR may be an important mechanism of action of oxyresveratrol. Moreover, a protection of motor function and cell loss seen in the in vivo model suggests that oxyresveratrol may be a useful therapeutic candidate for PD.-
dc.languageeng-
dc.publisherS Karger AG. The Journal's web site is located at http://www.karger.com/NDD-
dc.relation.ispartofNeurodegenerative Diseases-
dc.rightsNeurodegenerative Diseases. Copyright © S Karger AG.-
dc.titleOxyresveratrol mitigates cellular toxicity in an in-vitro and in-vivo model of Parkinson's disease-
dc.typeConference_Paper-
dc.identifier.emailHung, HLC: hungchl@hku.hk-
dc.identifier.emailChang, RCC: rccchang@hku.hk-
dc.identifier.authorityChang, RCC=rp00470-
dc.identifier.hkuros280643-
dc.identifier.volume17-
dc.identifier.issueSuppl 1-
dc.identifier.spage1470-
dc.identifier.epage1470-
dc.publisher.placeSwitzerland-

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