Elderberry diet enhances motor performance and reduces neuroinflammation-induced cell death in cerebellar ataxia rat models.

Apoptosis Astrogliosis Cerebellar ataxia Elderberry Microgliosis Motor coordination Neuroinflammation Neuroprotection

Journal

Journal of chemical neuroanatomy
ISSN: 1873-6300
Titre abrégé: J Chem Neuroanat
Pays: Netherlands
ID NLM: 8902615

Informations de publication

Date de publication:
22 Feb 2024
Historique:
received: 30 10 2023
revised: 06 02 2024
accepted: 07 02 2024
medline: 25 2 2024
pubmed: 25 2 2024
entrez: 24 2 2024
Statut: aheadofprint

Résumé

Cerebellar ataxia (CA) is a condition in which cerebellar dysfunction results in movement disorders such as dysmetria, synergy and dysdiadochokinesia. This study investigates the therapeutic effects of elderberry (EB) diet on the 3-acetylpyridine-induced (3-AP) CA rat model. First, CA rat models were generated by 3-AP administration followed by elderberry diet treatment containing 2% EB for 8 consecutive weeks. Motor performance, electromyographic activity and gene expression were then evaluated. The number of Purkinje neurons were evaluated by stereological methods. Immunohistochemistry for the microgliosis, astrogliosis and apoptosis marker caspase-3 was also performed. In addition, the morphology of microglia and astrocytes was assessed using the Sholl analysis method. The results showed that EB diet administration in a 3-AP ataxia model improved motor coordination, locomotor activity and neuro-muscular function, prevented Purkinje neurons degeneration, increased microglia and astrocyte complexity and reduced cell soma size. Moreover, EB diet administration decreased apoptosis in cerebellum of 3-AP ataxic model. In addition, elderberry diet treatment decreased the expression of inflammatory, apoptotic and necroptotic genes and increased the expression of antioxidant-related genes. The results suggest that the EB diet attenuates 3-AP-induced neuroinflammation leading to cell death and improves motor performance. Thus, the EB diet could be used as a therapeutic procedure for CA due to its neuroprotective effects.

Identifiants

pubmed: 38401660
pii: S0891-0618(24)00012-7
doi: 10.1016/j.jchemneu.2024.102399
pii:
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

102399

Informations de copyright

Copyright © 2024 Elsevier B.V. All rights reserved.

Déclaration de conflit d'intérêts

Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper. Conflict of interest The authors have no conflict of interest to declare.

Auteurs

Maryam Raoofi Nejad (M)

Department of Genetics, Faculty of Biological Sciences, North Tehran Branch, Islamic Azad University, Tehran, Iran. Electronic address: maryamraoofi1988@gmail.com.

Elham Siasi (E)

Department of Genetics, Faculty of Biological Sciences, North Tehran Branch, Islamic Azad University, Tehran, Iran. Electronic address: emi_biotech2006@yahoo.ca.

Mohammad Amin Abdollahifar (MA)

Department of Biology and Anatomical Sciences, School of Medicine, Shahid Beheshti University of Medical Sciences, Tehran, Iran. Electronic address: m_amin58@yahoo.com.

Abbas Aliaghaei (A)

Hearing Disorders Research Center, Loghman Hakim Hospital, Shahid Beheshti University of Medical Sciences, Tehran, Iran. Electronic address: abbas.aliaghaei@sbmu.ac.ir.

Elham Siasi (E)

Department of Genetics, Faculty of Biological Sciences, North Tehran Branch, Islamic Azad University, Tehran, Iran. Electronic address: aghaei60@gmail.com.

Classifications MeSH