Beta-Caryophyllene, a CB2R Selective Agonist, Protects Against Cognitive Impairment Caused by Neuro-inflammation and Not in Dementia Due to Ageing Induced by Mitochondrial Dysfunction.
Aging
/ drug effects
Aluminum Chloride
/ metabolism
Animals
Cognitive Dysfunction
/ metabolism
Dementia
/ metabolism
Disease Models, Animal
Galactose
/ metabolism
Hippocampus
/ drug effects
Lipid Peroxidation
Male
Maze Learning
/ drug effects
Mitochondrial Diseases
/ metabolism
Neuroinflammatory Diseases
/ metabolism
Neuroprotective Agents
/ pharmacology
Oxidative Stress
/ drug effects
Polycyclic Sesquiterpenes
/ pharmacology
Rats
Rats, Sprague-Dawley
D-galactose
aluminium chloride
cannabinoid 2
receptor.
chemobrain
cognitive impairment
doxorubicin
β-caryophyllene
Journal
CNS & neurological disorders drug targets
ISSN: 1996-3181
Titre abrégé: CNS Neurol Disord Drug Targets
Pays: United Arab Emirates
ID NLM: 101269155
Informations de publication
Date de publication:
2021
2021
Historique:
received:
30
07
2020
revised:
09
10
2020
accepted:
30
11
2020
pubmed:
4
2
2021
medline:
11
3
2022
entrez:
3
2
2021
Statut:
ppublish
Résumé
Dementia is a neurodegenerative disorder majorly evidenced by cognitive impairment. Although there are many types of dementia, the common underlying etiological factors in all the types are neuro-inflammation or aging induced apoptosis. β-caryophyllene, a cannabinoid type-2 receptor agonist, has been reported to have promising neuroprotective effects in cerebral ischemia and neuro-inflammation. In the present study, we evaluated the effects of β-caryophyllene against animal models of dementia whose etiology mimicked neuro-inflammation and aging. Two doses (50 and 100 mg/kg of body weight) of β-caryophyllene given orally were tested against AlCl β-caryophyllene, at both doses, showed significant improvement in memory when assessed using parameters like target quadrant entries, escape latency and path efficiency in the Morris water maze test for spatial memory. In the doxorubicin-induced chemobrain model, β-caryophyllene at 100 mg/kg significantly elevated acetylcholinesterase and catalase levels and lowered lipid peroxidation compared to the disease control. In the novel object recognition task, β-caryophyllene at 100 mg/kg significantly improved recognition index and discrimination index in the treated animals compared to the disease control, with a significant increase in catalase and a decrease in lipid peroxidation in both hippocampus and frontal cortex. However, in the D-galactose-induced mitochondrial dysfunction model, β-caryophyllene failed to show positive effects when spatial memory was assessed. It also failed to improve D-galactose-induced diminished mitochondrial complex I and II activities. Hence, we conclude that β-caryophyllene at 100 mg/kg protects against dementia induced by neuro-inflammation with no effect on neuronal aging induced by mitochondrial dysfunction.
Sections du résumé
BACKGROUND
Dementia is a neurodegenerative disorder majorly evidenced by cognitive impairment. Although there are many types of dementia, the common underlying etiological factors in all the types are neuro-inflammation or aging induced apoptosis. β-caryophyllene, a cannabinoid type-2 receptor agonist, has been reported to have promising neuroprotective effects in cerebral ischemia and neuro-inflammation.
OBJECTIVE
In the present study, we evaluated the effects of β-caryophyllene against animal models of dementia whose etiology mimicked neuro-inflammation and aging.
METHODS
Two doses (50 and 100 mg/kg of body weight) of β-caryophyllene given orally were tested against AlCl
RESULTS
β-caryophyllene, at both doses, showed significant improvement in memory when assessed using parameters like target quadrant entries, escape latency and path efficiency in the Morris water maze test for spatial memory. In the doxorubicin-induced chemobrain model, β-caryophyllene at 100 mg/kg significantly elevated acetylcholinesterase and catalase levels and lowered lipid peroxidation compared to the disease control. In the novel object recognition task, β-caryophyllene at 100 mg/kg significantly improved recognition index and discrimination index in the treated animals compared to the disease control, with a significant increase in catalase and a decrease in lipid peroxidation in both hippocampus and frontal cortex. However, in the D-galactose-induced mitochondrial dysfunction model, β-caryophyllene failed to show positive effects when spatial memory was assessed. It also failed to improve D-galactose-induced diminished mitochondrial complex I and II activities.
CONCLUSION
Hence, we conclude that β-caryophyllene at 100 mg/kg protects against dementia induced by neuro-inflammation with no effect on neuronal aging induced by mitochondrial dysfunction.
Identifiants
pubmed: 33530917
pii: CNSNDDT-EPUB-113860
doi: 10.2174/1871527320666210202121103
doi:
Substances chimiques
Neuroprotective Agents
0
Polycyclic Sesquiterpenes
0
Aluminum Chloride
3CYT62D3GA
caryophyllene
BHW853AU9H
Galactose
X2RN3Q8DNE
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
963-974Informations de copyright
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