ArticleBiological trace element research2026
Neuroprotective Potential of Chromium-D-Phenylalanine: Insights from Molecular Docking, Dynamics and Rotenone-Induced Parkinsonism in Rats.
Article in Biological trace element research, 2026. 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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2 citing papers in PubMed.
- Chromium(III) Beyond Insulin: A Mechanistic Roadmap Across the Energy-Redox-Inflammation Triad in Obesity and Cardiometabolic Disease.Biological trace element research · 2026Review
- Article
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5 authors.
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Abstract
This study investigates the neuroprotective potential of Chromium-D-Phenylalanine [Cr(D-Phe)₃] using molecular docking, molecular dynamics (MD) simulations and an in vivo rotenone-induced Parkinsonism model in rats. Molecular docking revealed a strong binding affinity between Cr(D-Phe)₃ and α-synuclein (PDB ID: 1XQ8), with a docking score of -8.9 kcal/mol, surpassing Levodopa (-7.7 kcal/mol). MD simulations further confirmed the stability of the Cr(D-Phe)₃-α-synuclein complex, demonstrating minimal RMSD fluctuations and sustained structural compactness over a 100-ns simulation period. In in vivo study in rats, Cr(D-Phe)₃ was administered orally at doses of 20, 40 and 80 µg/kg. The 40 µg/kg dose exhibited the most pronounced neuroprotective effects. Behavioural assessments showed significant improvement, with a 13.4% (p < 0.05) reduction in catalepsy duration, a 173.7% (p < 0.01) increase in locomotor activity and a 207.6% (p < 0.01) enhancement in neuromuscular coordination compared to the rotenone-treated group. Biochemical analyses demonstrated substantial restoration of antioxidant defences, with catalase levels increasing by 14.3% (p < 0.05) and GSH levels by 104.6% (p < 0.01). Oxidative and nitrative stress markers were significantly reduced, with lipid peroxidation decreasing by 22.7% (p < 0.001) and nitrite levels by 26.3% (p < 0.001). Furthermore, Cr(D-Phe)₃ effectively suppressed neuroinflammation, lowering TNF-α levels by 35.5% (p < 0.001), while dopamine levels were restored by 45.4% (p < 0.001) compared to rotenone-treated rats. Histopathological analysis confirmed the preservation of neuronal integrity in the substantia nigra and cortical regions. These findings suggest that Cr(D-Phe)₃ mitigates Parkinsonism-associated neurodegeneration by reducing oxidative stress, suppressing neuroinflammation and preserving dopaminergic neuronal function. Cr(D-Phe)₃ holds promise as a potential therapeutic candidate for Parkinsonism, warranting further investigation.
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