Neuroinflammation and Behavioral Deficit in Rotenone-Induced Neurotoxicity in Rats and the Possible Effects of Butanolic Extract of
Centaurea africana
Rotenone
apoptosis
n-BuOH extract
neuroinflammation.
rats
Journal
Recent advances in inflammation & allergy drug discovery
ISSN: 2772-2716
Titre abrégé: Recent Adv Inflamm Allergy Drug Discov
Pays: Netherlands
ID NLM: 101776469
Informations de publication
Date de publication:
2022
2022
Historique:
received:
26
08
2021
revised:
12
12
2021
accepted:
27
12
2021
pubmed:
7
1
2022
medline:
9
3
2022
entrez:
6
1
2022
Statut:
ppublish
Résumé
Many studies have used rotenone (ROT) to create an experimental animal model of Parkinson's disease (PD) because of its ability to induce similar behavioral and motor deficits. PD is the most common age-related motoric neurodegenerative disorder. Neuroinflammation and apoptosis play an important role in the pathogenesis of this disease. This study investigated the effect of butanolic (n-BuOH) extract of Centaurea africana (200 mg/kg, 16 days) on a ROT-induced neurotoxicity model in male Wistar albino rats. Estimation of Tumor Necrosis Factor (TNF-α) and Nitric Oxide (NO) levels along with the myeloperoxidase (MPO) activity in brains was carried out in order to evaluate neuro-inflammation. Oxidative stress, Caspase 3 activity (apoptosis), and behavioral alterations were also evaluated. In behavior assessment, using Ludolph Movement Analysis Scale, all ROT treated animals showed a decreased locomotor activity. The mitochondrial dysfunction induced by ROT was expressed by a decreased activity of complex I of the mitochondrial respiratory chain and increased lipid peroxidation and caspase 3. Co-treatment with the n-BuOH extract significantly restored the activity of complex I (65.41 %) compared to treatment with ROT alone. The n-BuOH extract also reduced the neuroinflammation in rat brains by reducing MPO activity (75.12 %), NO levels (77.43 %), and TNF-α (71.48 %) compared to the group treated with ROT. The obtained results indicated that C. africana n-BuOH extract exhibited a protective effect in rats.
Sections du résumé
BACKGROUND
BACKGROUND
Many studies have used rotenone (ROT) to create an experimental animal model of Parkinson's disease (PD) because of its ability to induce similar behavioral and motor deficits. PD is the most common age-related motoric neurodegenerative disorder. Neuroinflammation and apoptosis play an important role in the pathogenesis of this disease.
OBJECTIVE
OBJECTIVE
This study investigated the effect of butanolic (n-BuOH) extract of Centaurea africana (200 mg/kg, 16 days) on a ROT-induced neurotoxicity model in male Wistar albino rats.
METHODS
METHODS
Estimation of Tumor Necrosis Factor (TNF-α) and Nitric Oxide (NO) levels along with the myeloperoxidase (MPO) activity in brains was carried out in order to evaluate neuro-inflammation. Oxidative stress, Caspase 3 activity (apoptosis), and behavioral alterations were also evaluated.
RESULTS
RESULTS
In behavior assessment, using Ludolph Movement Analysis Scale, all ROT treated animals showed a decreased locomotor activity. The mitochondrial dysfunction induced by ROT was expressed by a decreased activity of complex I of the mitochondrial respiratory chain and increased lipid peroxidation and caspase 3. Co-treatment with the n-BuOH extract significantly restored the activity of complex I (65.41 %) compared to treatment with ROT alone. The n-BuOH extract also reduced the neuroinflammation in rat brains by reducing MPO activity (75.12 %), NO levels (77.43 %), and TNF-α (71.48 %) compared to the group treated with ROT.
CONCLUSION
CONCLUSIONS
The obtained results indicated that C. africana n-BuOH extract exhibited a protective effect in rats.
Identifiants
pubmed: 34986781
pii: RAIAD-EPUB-119992
doi: 10.2174/2772270816666220105124730
doi:
Substances chimiques
Neuroprotective Agents
0
Plant Extracts
0
Rotenone
03L9OT429T
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
35-43Subventions
Organisme : Algerian Ministry of Higher Education and Scientific Research
ID : D01N01UN250 120190002
Informations de copyright
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