PUBLICATION

Oral Delivery of a Nanocrystal Formulation of Schisantherin A with Improved Bioavailability and Brain Delivery for the Treatment of Parkinson's Disease

Authors
Chen, T., Li, C., Li, Y., Xiang, Y., Lee, S.M., Zheng, Y.
ID
ZDB-PUB-161016-7
Date
2016
Source
Molecular pharmaceutics   13(11): 3864-3875 (Journal)
Registered Authors
Keywords
none
MeSH Terms
  • Administration, Oral
  • Animals
  • Brain/drug effects
  • Brain/metabolism
  • Cyclooctanes/administration & dosage*
  • Cyclooctanes/chemistry
  • Cyclooctanes/therapeutic use*
  • Dioxoles/administration & dosage*
  • Dioxoles/chemistry
  • Dioxoles/therapeutic use*
  • Disease Models, Animal
  • Drug Compounding/methods*
  • Lignans/administration & dosage*
  • Lignans/chemistry
  • Lignans/therapeutic use*
  • Male
  • Nanoparticles/chemistry*
  • Parkinson Disease/drug therapy*
  • Parkinson Disease/metabolism
  • Rats, Sprague-Dawley
  • Zebrafish
PubMed
27740776 Full text @ Mol. Pharm.
Abstract
Schisantherin A (SA) is a promising anti-Parkinsonism Chinese herbal medicine but with poor water solubility and challenges to be delivered to the brain. We formulated SA as nanocrystals (SA-NC), aiming to improve its solubility and pharmacokinetic profile and thus provide a potential therapeutic agent for the treatment of Parkinson's disease (PD). The rod-shaped SA-NC had a particle size of ∼160 nm with 33.3% drug loading, and the nanocrystals exhibited a fast dissolution rate in vitro. The intact drug nanocrystals could be internalized into Madin-Darby canine kidney (MDCK) cells, which were followed by rapid intracellular release, and most of the drug was transported to the basolateral side in its soluble form. Following oral administration of the SA-NC or an SA suspension, the accumulated concentration of the SA-NC in the plasma and brain was considerably higher than that observed for the SA suspension, but the drug targeting efficiency was similar. The SA-NC significantly reversed the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced dopaminergic (DA) neuronal loss and locomotion deficiency in zebrafish, as well as the 1-methyl-4-phenylpyridinium ion (MPP+)-induced damage of neuronal cell culture model. Further Western blot analysis demonstrated that the stronger neuroprotective effect of SA-NC may be partially mediated by the activation of the protein kinase B (Akt)/glycogen synthase kinase-3β (Gsk3β) pathway. Taken together, these data provide solid evidence that the nanocrystal formulation has the potential to improve the bioavailability and brain concentration of this Biopharmaceutics Classification System (BCS) class II compound, SA, for the treatment of PD.
Genes / Markers
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Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Antibodies
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Mapping