Melittin ameliorates motor function and prevents autophagy-induced cell death and astrogliosis in rat models of cerebellar ataxia induced by 3-acetylpyridine.
Autophagy
Cerebellar ataxia
Locomotion
Melittin
Neuroprotection
Journal
Neuropeptides
ISSN: 1532-2785
Titre abrégé: Neuropeptides
Pays: Netherlands
ID NLM: 8103156
Informations de publication
Date de publication:
Dec 2022
Dec 2022
Historique:
received:
24
08
2022
revised:
10
10
2022
accepted:
11
10
2022
pubmed:
25
10
2022
medline:
15
11
2022
entrez:
24
10
2022
Statut:
ppublish
Résumé
Cerebellar ataxia (CA) is a form of ataxia that adversely affects the cerebellum. This study aims to investigate the therapeutic effects of melittin (MEL) on a 3-acetylpyridine-induced (3-AP) cerebellar ataxia (CA) rat model. Initially, CA rat models were generated by 3-AP administration followed by the subcutaneous injection of MEL. The open-field test was used for the evaluation of locomotion and anxiety. Immunohistochemistry was also conducted for the autophagy markers of LC3 and Beclin1. In the next step, the morphology of the astrocyte, the cell responsible for maintaining homeostasis in the CNS, was evaluated by the Sholl analysis. The findings suggested that the administration of MEL in a 3-AP model of ataxia improved locomotion and anxiety (P < 0.001), decreased the expression of LC3 (P < 0.01) and Beclin1 (P < 0.05), increased astrocyte complexity (P < 0.05) and reduced astrocyte cell soma size (P < 0.001). Overall, the findings imply that the MEL attenuates the 3-AP-induced autophagy, causes cell death and improves motor function. As such, it could be used as a therapeutic procedure for CA due to its neuroprotective effects.
Sections du résumé
BACKGROUND
BACKGROUND
Cerebellar ataxia (CA) is a form of ataxia that adversely affects the cerebellum. This study aims to investigate the therapeutic effects of melittin (MEL) on a 3-acetylpyridine-induced (3-AP) cerebellar ataxia (CA) rat model.
METHODS
METHODS
Initially, CA rat models were generated by 3-AP administration followed by the subcutaneous injection of MEL. The open-field test was used for the evaluation of locomotion and anxiety. Immunohistochemistry was also conducted for the autophagy markers of LC3 and Beclin1. In the next step, the morphology of the astrocyte, the cell responsible for maintaining homeostasis in the CNS, was evaluated by the Sholl analysis.
RESULTS
RESULTS
The findings suggested that the administration of MEL in a 3-AP model of ataxia improved locomotion and anxiety (P < 0.001), decreased the expression of LC3 (P < 0.01) and Beclin1 (P < 0.05), increased astrocyte complexity (P < 0.05) and reduced astrocyte cell soma size (P < 0.001).
CONCLUSIONS
CONCLUSIONS
Overall, the findings imply that the MEL attenuates the 3-AP-induced autophagy, causes cell death and improves motor function. As such, it could be used as a therapeutic procedure for CA due to its neuroprotective effects.
Identifiants
pubmed: 36280441
pii: S0143-4179(22)00070-1
doi: 10.1016/j.npep.2022.102295
pii:
doi:
Substances chimiques
3-acetylpyridine
00QT8FX306
Beclin-1
0
Melitten
20449-79-0
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
102295Informations de copyright
Copyright © 2022 Elsevier Ltd. All rights reserved.
Déclaration de conflit d'intérêts
Declaration of Competing Interest The authors declare that they have no conflict of interest.