Molecular Docking, Drug-Likeness and Toxicity Prediction to Determine the Role of the Taxifolin on Neurological Diseases
Abstract:
Through an in-silico approach, the effects of
taxifolin on tau, alpha 2 macroglobulin (A2M) and alpha 1 anti-chymotrypsin
(ACT), proteins are investigated in relation to neurological disorders. In
order to facilitate protein interaction, the ligand taxifolin (extracted from
the PubChem Database) and protein receptor molecules (extracted from the PDB)
are prepared, converted to PDBQT format, and uploaded in an auto dock. The
effects of taxifolin on tau protein, ACT, and A2M are still being studied, but
the preliminary findings are promising. These interactions suggest that
taxifolin may have a complex role in controlling neuroinflammation,
proteostasis, and neurodegeneration in neurological illnesses due to their
substantial binding affinity for tau, ACT, and A2M protein. Taxifolin shows
promise as a therapy for neurological disorders by targeting tau protein, ACT,
and A2M. Lipinski's Rule states that Taxifolin administered orally should not
violate more than one condition. Taxifolin examined was in category IV, which
is under the dosage of 300 < LD50 = 2000 mg/kg. A significant root mean
square value was 0.000, with a docking score of -7.2 for alpha 1
antichymotrypsin and taxifolin. Interactions in 2D and 3D include conventional
hydrogen bonds, carbon-hydrogen bonds, and unfavourable donor-donor
interactions. The chosen root mean square value was associated with a
significant docking score of -10.2 for alpha2 macroglobulin and taxifolin. The
docking score for alpha 2 macroglobulin in a two-dimensional structure, emphasising
pi-donor bonds, unfavourable donor-donor interactions, and conventional
carbon-hydrogen connections. According to these findings, taxifolin has a
significant affinity for alpha 2 macroglobulin. Tau had a high root mean square
value and a docking score of -7.5 with tau protein. Tau's 2D and 3D structures
contain pi-alkyl contacts, pi-stacking interactions, unfavourable donor-donor
interactions, and carbon-hydrogen bonds. Its ability to raise A2M activity,
decrease ACT expression, and stop tau protein aggregation suggests a variety of
potential neuroprotective benefits.
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