Please use this identifier to cite or link to this item: http://hdl.handle.net/10397/115212
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dc.contributorDepartment of Food Science and Nutrition-
dc.creatorBi, D-
dc.creatorHuang, J-
dc.creatorZhu, N-
dc.creatorCao, J-
dc.creatorWu, Y-
dc.creatorYao, L-
dc.creatorDing, X-
dc.creatorWu, J-
dc.creatorCao, X-
dc.creatorXu, X-
dc.date.accessioned2025-09-15T02:22:58Z-
dc.date.available2025-09-15T02:22:58Z-
dc.identifier.urihttp://hdl.handle.net/10397/115212-
dc.language.isoenen_US
dc.publisherElsevier BVen_US
dc.rights© 2025 The Authors. Published by Elsevier B.V. This is an open access article under the CC BY license (http://creativecommons.org/licenses/by/4.0/).en_US
dc.rightsThe following publication Bi, D., Huang, J., Zhu, N., Cao, J., Wu, Y., Yao, L., Ding, X., Wu, J., Cao, X., & Xu, X. (2025). Neuroprotective effect of an unsaturated mannuronate oligosaccharide derived from enzyme-degraded polymannuronate on an in vitro Parkinson's disease-like model. Journal of Agriculture and Food Research, 22, 101994 is available at https://doi.org/10.1016/j.jafr.2025.101994.en_US
dc.subjectAnti-apoptosisen_US
dc.subjectAntioxidanten_US
dc.subjectAutophagyen_US
dc.subjectCell culture modelen_US
dc.subjectParkinson’s disease (PD)en_US
dc.subjectUnsaturated mannuronate oligosaccharide (MOS)en_US
dc.titleNeuroprotective effect of an unsaturated mannuronate oligosaccharide derived from enzyme-degraded polymannuronate on an in vitro Parkinson's disease-like modelen_US
dc.typeJournal/Magazine Articleen_US
dc.identifier.volume22-
dc.identifier.doi10.1016/j.jafr.2025.101994-
dcterms.abstractThis study mainly aimed to explore the intervention effect of an unsaturated mannuronate oligosaccharide (MOS) on Parkinson's disease (PD) and its potential mechanism at the cellular level. MOS, which possesses high water solubility and excellent biocompatibility, was prepared by enzyme degradation of alginate-derived polymannuronate. In 6-hydroxydopamine (6-OHDA)-induced SH-SY5Y cell culture, MOS treatment effectively augmented the expression of tyrosine hydroxylase (TH), PTEN-induced putative kinase 1 (PINK1) and parkin but suppressed the expression of α-synuclein (α-syn). Moreover, MOS exerted antioxidant activity by suppressing the excessive generation of reactive oxygen species and enhancing the activity of superoxide dismutase. MOS also inhibited 6-OHDA-induced apoptosis by enhancing mitochondrial membrane potential and mitigating the Bax/Bcl-2 pathway and improving autophagy that was blocked by 6-OHDA. In summary, these results have demonstrated the significant neuroprotective effect of MOS on SH-SY5Y cells, indicating that MOS has a certain intervention effect on the development of PD. This provides a promising foundation for developing novel therapeutic strategies targeting neurodegenerative disorders.-
dcterms.accessRightsopen accessen_US
dcterms.bibliographicCitationJournal of agriculture and food research, Aug. 2025, v. 22, 101994-
dcterms.isPartOfJournal of agriculture and food research-
dcterms.issued2025-08-
dc.identifier.scopus2-s2.0-105005578686-
dc.identifier.eissn2666-1543-
dc.identifier.artn101994-
dc.description.validate202509 bcch-
dc.description.oaVersion or Recorden_US
dc.identifier.FolderNumberOA_Scopus/WOSen_US
dc.description.fundingSourceOthersen_US
dc.description.fundingTextThis work was supported financially by the National Natural Science Foundation of China (32172193 and 32302058), the National Key Research and Development Program of China (2024YFD2401605 and 2023YFF1001200), the Shenzhen Science and Technology Program (JCYJ20240813142721028), the Project of DEGP (2023ZDZX4047), Guangdong Science and Technology Planning Project (2020B121202014), and Natural Science Foundation of Shenzhen University General Hospital (SUGH2018QD005).en_US
dc.description.pubStatusPublisheden_US
dc.description.oaCategoryCCen_US
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