ArticleNeurochemical research2025
Possible Mitigating Effect of Nobiletin on Rotenone-Induced Parkinsonism in Male Albino Rat Model: Targeting Bmal1/Nrf2 Mediated Ferroptosis and Restoring Mitochondrial Mitophagy.
Article in Neurochemical research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
3 citing papers in PubMed.
- The mitophagy-inflammasome axis: a shared pathological hub in Alzheimer's and Parkinson's diseases.Translational neurodegeneration · 2026Review
- Global evolution of ferroptosis research: a comprehensive bibliometric analysis of publication trends, geographic patterns, pharmacological innovation, and translational progress from inception through 2025.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Potential and Mechanism of Nobiletin in Diabetes Mellitus and Associated Complications.Pharmaceuticals (Basel, Switzerland) · 2025Review
Corrections and comments
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Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Ferroptosis and circadian disruption might be implicated in Parkinson disease (PD), a neurodegenerative disorder due to degeneration of dopaminergic neurons in the substantia nigra. As such, the ability to preserve mitochondrial and therefore neuronal homeostasis is essential. In PD, Nobiletin (NOB) may have neuroprotective effects. Still, further clarification is needed about the processes behind these impacts. To evaluate the positive effect of NOB against rotenone induced PD in rats via the Bmal1/ NRF2 axis regulation. Four groups of thirty-two male Albino rats were randomly assigned: Control, NOB treated, rotenone treated, and combined Rotenone and NOB treated groups. The validation of the neuroprotective potential of NOB entailed a behavioral examination, RT-PCR and colorimetric evaluation of biochemical markers, as well as immunohistopathological study of brain tissues. The relative gene expression of Bmal1 increased with NOB therapy significantly reducing the circadian rhythm disruption. Furthermore, as shown by the elevated Nrf2-DNA binding activity, increased levels of GPx4, and decreased levels of GSH with comparable low levels of MDA and Fe
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.