Article3 Biotech2025
Targeting dopaminergic neuronal death: Luteolin as a therapeutic modulator in Parkinson's disease.
Article in 3 Biotech, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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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.
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Who cites it
6 citing papers in PubMed.
- Luteolin and glycitein from Codonopsis pilosula ameliorate age-related locomotor decline in C. elegans via DAF-16-dependent but autophagy-divergent pathways.Biogerontology · 2026Article
- Zein-Pectin Nanoparticles for Luteolin Delivery: Physicochemical Characterization, Antioxidant Activity, and Simulated Gastrointestinal Behavior.Journal of food science · 2026Article
- Luteolin and neuroinflammation: a multi-target therapeutic strategy for central nervous system disorders.Frontiers in pharmacology · 2026Review
- Luteolin as a dietary flavonoid for brain health: modulating neuroinflammation and cognitive decline in neurodegenerative disorders.Frontiers in nutrition · 2026Review
- Flavonoids improve neurotransmitters for Parkinson's treatment: mechanism and therapeutic potential.Frontiers in pharmacology · 2026Review
- In Vitro Antioxidant Activity and In Vivo Neuroprotective Effect ofAntioxidants (Basel, Switzerland) · 2025Article
Corrections and comments
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Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Understanding the convoluted roles of dopamine in brain function is supreme for elucidating the pathophysiology and the therapeutic approach of movement disorders. Of which, Parkinson's disease (PD) is a progressive neurological ailment characterized by disturbed motor and non-motor functions. Luteolin, a plant-derived flavonoid, exhibits neuroprotective properties through its antioxidant and anti-inflammatory effects. In this study, we evaluated the therapeutic potential of luteolin in a rotenone-induced Wistar rat model of PD. Results of behavior assessment showed that luteolin (25 mg/kg and 50 mg/kg i.p.) treatment for 28 days significantly and dose-dependently improved motor functions. Furthermore, biochemical analysis demonstrated that luteolin restored oxidative balance by elevating glutathione (GSH) levels and reducing nitrate content. Additionally, ELISA results indicated that luteolin modulated level of tumor necrosis factor-alpha (TNF-α) and Bax, thereby reducing inflammation and neuronal apoptosis. Moreover, dopamine levels were significantly increased in rat brain homogenate, corroborating the neuroprotective effects of luteolin. Histopathological analysis further confirmed dopaminergic neuronal preservation in the cortex. These findings suggest that luteolin may serve as a potential therapeutic candidate for PD by mitigating oxidative stress, neuroinflammation, and apoptosis.
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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 Socratic graph.