ArticleInflammopharmacology2025
Neuroprotective efficacy of berberine and caffeine against rotenone-induced neuroinflammatory and oxidative disturbances associated with Parkinson's disease via inhibiting α-synuclein aggregation and boosting dopamine release.
Article in Inflammopharmacology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed.
- Phytomedicines in preclinical and clinical research on antipsychotics-induced EPS/EPS-like behaviors: therapeutic effects and neurobiological mechanisms.Frontiers in psychiatry · 2026Review
- Caffeine in Aging Brains: Cognitive Enhancement, Neurodegeneration, and Emerging Concerns About Addiction.International journal of environmental research and public health · 2025Review
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Authors and funding
4 authors.
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Abstract
Parkinson's disease (PD) is characterized by motor impairment, glial-mediated inflammation, redox imbalance, and α-synuclein (α-syn) aggregation. Conventional therapies relieve early PD symptoms, but they do not repair dopaminergic neurons. Berberine (BBR) and caffeine (CAF), both natural alkaloids, exhibited neuroprotective effects in many neurodegenerative disorders. Consequently, we hypothesized that the combination of BBR and CAF therapies would offer protection against PD-related impairments in the rotenone (ROT)-induced rat model when compared to the commercial drug, metformin (MTF). Our results showed that the combined administration of BBR (25 mg/kg/day) and CAF (2.5 mg/kg/day) for four weeks prevented motor deficits, weight reduction, dopamine (DA) depletion, and monoamine oxidase (MAO) activity in ROT-induced rats in comparison with monotherapy of BBR and CAF along with MTF. This combination produced a notable neuroprotective effect by reducing tumor necrosis factor (TNF)-α and interleukin-16 (IL-6) in midbrain of rats. BBR and CAF combinations markedly normalized tyrosine hydroxylase (TH) levels and decreased total α-syn and α-syn-p
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