ArticleMarine drugs2016
Neuroprotective Effect of the Marine-Derived Compound 11-Dehydrosinulariolide through DJ-1-Related Pathway in In Vitro and In Vivo Models of Parkinson's Disease.
Article in Marine drugs, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed, 55 citations in OpenAlex.
- The Neuroprotective Effects of the Crinoid Natural Compound Rhodoptilometrin in Parkinson's Disease Experimental Models: Implications for ER Stress and Autophagy Modulation.ACS chemical neuroscience · 2025Article
- Soft Corals-derived Dihydrosinularin Attenuates Neuronal Apoptosis in 6-hydroxydopamine-induced Cell Model of Parkinson's Disease by Regulating the PI3K Pathway.Current medicinal chemistry · 2025Article
- Unraveling Dysregulated Cell Signaling Pathways, Genetic and Epigenetic Mysteries of Parkinson's Disease.Molecular neurobiology · 2024Review
- A Complex Interplay of DJ-1, LRRK2, and Nrf2 in the Regulation of Mitochondrial Function in Cypermethrin-Induced Parkinsonism.Molecular neurobiology · 2024Article
- Marine-Derived Components: Can They Be a Potential Therapeutic Approach to Parkinson's Disease?Marine drugs · 2023Review
- Neuroprotective effects of a lead compound from coral via modulation of the orphan nuclear receptor Nurr1.CNS neuroscience & therapeutics · 2023Article
- The Neuroprotective Effect of Isotetrandrine on Parkinson's Disease via Anti-Inflammation and AntiapoptosisParkinson's disease · 2023Article
- Precision Medicine in Parkinson's Disease: From Genetic Risk Signals to Personalized Therapy.Brain sciences · 2022Review
- A MajorPlants (Basel, Switzerland) · 2022Article
- Pinocembrin ameliorates atrial fibrillation susceptibility in rats with anxiety disorder induced by empty bottle stimulation.Frontiers in pharmacology · 2022Article
- Review
- Benefits under the Sea: The Role of Marine Compounds in Neurodegenerative Disorders.Marine drugs · 2021Review
- Pharmacological Modulation of Nrf2/HO-1 Signaling Pathway as a Therapeutic Target of Parkinson's Disease.Frontiers in pharmacology · 2021Review
- Neuroprotective Effects of Estradiol plus Lithium Chloride via Anti-Apoptosis and Neurogenesis Pathway inParkinson's disease · 2021Article
- Modeling Parkinson's Disease: Not Only Rodents?Frontiers in aging neuroscience · 2021Article
- The Antioxidant, Anti-Inflammatory, and Neuroprotective Properties of the Synthetic Chalcone Derivative AN07.Molecules (Basel, Switzerland) · 2020Article
- A new multigene HCIQ subfamily from the sea anemone Heteractis crispa encodes Kunitz-peptides exhibiting neuroprotective activity against 6-hydroxydopamine.Scientific reports · 2020Article
- Amelioration of Mitochondrial Quality Control and Proteostasis by Natural Compounds in Parkinson's Disease Models.International journal of molecular sciences · 2019Review
- In Vitro and In Vivo Neuroprotective Effects of Stellettin B Through Anti-Apoptosis and the Nrf2/HO-1 Pathway.Marine drugs · 2019Article
- Fishing in the Cell Powerhouse: Zebrafish as A Tool for Exploration of Mitochondrial Defects Affecting the Nervous System.International journal of molecular sciences · 2019Review
Corrections and comments
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Authors and funding
13 authors at 6 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Parkinson's disease (PD) is a neurodegenerative disorder characterized by tremor, rigidity, bradykinesia, and gait impairment. In a previous study, we found that the marine-derived compound 11-dehydrosinulariolide (11-de) upregulates the Akt/PI3K pathway to protect cells against 6-hydroxydopamine (6-OHDA)-mediated damage. In the present study, SH-SY5Y, zebrafish and rats were used to examine the therapeutic effect of 11-de. The results revealed the mechanism by which 11-de exerts its therapeutic effect: the compound increases cytosolic or mitochondrial DJ-1 expression, and then activates the downstream Akt/PI3K, p-CREB, and Nrf2/HO-1 pathways. Additionally, we found that 11-de could reverse the 6-OHDA-induced downregulation of total swimming distance in a zebrafish model of PD. Using a rat model of PD, we showed that a 6-OHDA-induced increase in the number of turns, and increased time spent by rats on the beam, could be reversed by 11-de treatment. Lastly, we showed that 6-OHDA-induced attenuation in tyrosine hydroxylase (TH), a dopaminergic neuronal marker, in zebrafish and rat models of PD could also be reversed by treatment with 11-de. Moreover, the patterns of DJ-1 expression observed in this study in the zebrafish and rat models of PD corroborated the trend noted in previous in vitro studies.
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