Epigallocatechin-3-gallate PEGylated poly(lactic-co-glycolic) acid nanoparticles mitigate striatal pathology and motor deficits in 3-nitropropionic acid intoxicated mice

Author:

Cano Amanda123ORCID,Ettcheto Miren345,Espina Marta12,Auladell Carmen6,Folch Jaume35,Kühne Britta A4,Barenys Marta4,Sánchez-López Elena123ORCID,Souto Eliana B78,García Maria Luisa12,Turowski Patric9,Camins Antonio34

Affiliation:

1. Department of Pharmacy, Pharmaceutical Technology & Physical Chemistry, Faculty of Pharmacy & Food Sciences, University of Barcelona, Barcelona, Spain

2. Institute of Nanoscience & Nanotechnology (IN2UB), Barcelona, Spain

3. Biomedical Research Networking Centre in Neurodegenerative Diseases (CIBERNED), Madrid, Spain

4. Department of Pharmacology, Toxicology & Therapeutic Chemistry, Faculty of Pharmacy & Food Sciences, University of Barcelona, Spain

5. Unit of Biochemistry & Pharmacology, Faculty of Medicine & Health Sciences, University of Rovira i Virgili, Reus (Tarragona), Spain

6. Department of Cellular Biology, Physiology & Immunology, Faculty of Biology, University of Barcelona, Spain

7. Department of Pharmaceutical Technology, Faculty of Pharmacy, University of Coimbra, Coimbra, Portugal

8. CEB – Centre of Biological Engineering, University of Minho, Campus de Gualtar 4710-057 Braga, Portugal

9. UCL Institute of Ophthalmology, University College of London, London, UK

Abstract

Aim: To compare free and nanoparticle (NP)-encapsulated epigallocatechin-3-gallate (EGCG) for the treatment of Huntington’s disease (HD)-like symptoms in mice. Materials & methods: EGCG was incorporated into PEGylated poly(lactic-co-glycolic) acid NPs with ascorbic acid (AA). HD-like striatal lesions and motor deficit were induced in mice by 3-nitropropionic acid-intoxication. EGCG and EGCG/AA NPs were co-administered and behavioral motor assessments and striatal histology performed after 5 days. Results: EGCG/AA NPs were significantly more effective than free EGCG in reducing motor disturbances and depression-like behavior associated with 3-nitropropionic acid toxicity. EGCG/AA NPs treatment also mitigated neuroinflammation and prevented neuronal loss. Conclusion: NP encapsulation enhances therapeutic robustness of EGCG in this model of HD symptomatology. Together with our previous findings, this highlights the potential of EGCG/AA NPs in the symptomatic treatment of neurodegenerative diseases.

Publisher

Future Medicine Ltd

Subject

Development,General Materials Science,Biomedical Engineering,Medicine (miscellaneous),Bioengineering

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