Neuroprotective effects of Ellagic acid against acrylamide-induced neurotoxicity in rats.
Acrylamide
/ toxicity
Animals
Brain
/ drug effects
Cognition
/ drug effects
Ellagic Acid
/ pharmacology
Exploratory Behavior
/ drug effects
Inflammation
/ drug therapy
Male
Motor Activity
/ drug effects
Neurons
/ drug effects
Neuroprotective Agents
/ pharmacology
Oxidative Stress
/ drug effects
Rats, Wistar
Acrylamide
Ellagic acid
neurotoxicity
rat
Journal
Neurological research
ISSN: 1743-1328
Titre abrégé: Neurol Res
Pays: England
ID NLM: 7905298
Informations de publication
Date de publication:
May 2019
May 2019
Historique:
pubmed:
9
2
2019
medline:
19
4
2019
entrez:
9
2
2019
Statut:
ppublish
Résumé
Acrylamide (ACR) is an environmental contaminant and a well-known neurotoxin. Ellagic acid (EA), a natural plant polyphenol, has shown a variety of beneficial effects. The present study was designed to explore whether EA could attenuate ACR-induced neurotoxicity in rats and to explore the underlying mechanisms. Animals were divided into five groups. Group 1 was treated with normal saline (2 mL/kg) for 30 days. Group 2 was treated with ACR (20 mg/kg, orally) for 30 days. Groups 3 and 4 were treated with ACR and EA (10 and 30 mg/kg, orally) for 30 days. Group 5 was treated with EA (30 mg/kg, orally) for 30 days. Open field, rotarod and passive avoidance test were conducted to evaluate behavioral changes, respectively. The brain cortex was used for histological examination. Different oxidative parameters and inflammatory biomarkers were assessed in the brain cortex. ACR-administered rats showed a considerable impairment in exploratory behavior, motor performance as well as cognition. Our data also showed that ACR administration significantly increases malondialdehyde, nitric oxide, interleukin-1β and tumor necrosis factor-α levels. Moreover, it decreases brain glutathione level, superoxide dismutase, glutathione peroxidase, catalase activity. Co-administration of EA (especially 30 mg/kg, p.o.) prevented these changes; however, it did not affect the glutathione peroxidase activity. These results were supported by histopathological observations of the brain. Our results suggest that EA can be useful for protecting brain tissue against ACR-induced neurotoxicity through ameliorative effects on inflammatory indices and oxidative stress parameters.
Identifiants
pubmed: 30735102
doi: 10.1080/01616412.2019.1576319
doi:
Substances chimiques
Neuroprotective Agents
0
Ellagic Acid
19YRN3ZS9P
Acrylamide
20R035KLCI
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM