Hexahydrocurcumin alleviated blood-brain barrier dysfunction in cerebral ischemia/reperfusion rats.
Animals
Aquaporin 4
/ metabolism
Blood-Brain Barrier
/ drug effects
Brain
/ blood supply
Brain Edema
/ drug therapy
Brain Ischemia
/ metabolism
Curcumin
/ analogs & derivatives
Infarction
/ drug therapy
Infarction, Middle Cerebral Artery
Male
Rats
Rats, Wistar
Reperfusion Injury
/ drug therapy
Zonula Occludens-1 Protein
/ metabolism
Blood–brain barrier
Cerebral edema
Cerebral ischemia/reperfusion
Neutrophil infiltration
Tight junction proteins
Journal
Pharmacological reports : PR
ISSN: 2299-5684
Titre abrégé: Pharmacol Rep
Pays: Switzerland
ID NLM: 101234999
Informations de publication
Date de publication:
Jun 2020
Jun 2020
Historique:
received:
21
07
2019
accepted:
11
12
2019
revised:
22
11
2019
pubmed:
13
2
2020
medline:
13
4
2021
entrez:
13
2
2020
Statut:
ppublish
Résumé
Hexahydrocurcumin (HHC), a major metabolite of curcumin, has been reported to have protective effects against ischemic and reperfusion damage. The goal of the present research was to examine whether HHC could alleviate brain damage and ameliorate functional outcomes by diminishing the blood-brain barrier (BBB) damage that follows cerebral ischemia/reperfusion. Middle cerebral artery occlusion was induced for 2 h in rats followed by reperfusion. The rats were divided into three groups: sham-operated, vehicle-treated, and HHC-treated groups. At the onset of reperfusion, the rats were immediately intraperitoneally injected with 40 mg/kg HHC. At 48 h after reperfusion, the rats were evaluated for neurological deficits and TTC staining. At 24 h and 48 h after reperfusion, animals were sacrificed, and their brains were extracted. Treatment with HHC reduced neurological scores, infarct volume, morphological changes, Evans blue leakage and immunoglobulin G extravasation. Moreover, HHC treatment reduced BBB damage and neutrophil infiltration, downregulated myeloperoxidase, ICAM-1, and VCAM-1, upregulated tight junction proteins (TJPs), and reduced aquaporin 4 expression and brain water content. These results revealed that HHC treatment preserved the BBB from cerebral ischemia/reperfusion injury by regulating TJPs, attenuating neutrophil infiltration, and reducing brain edema formation.
Sections du résumé
BACKGROUND
BACKGROUND
Hexahydrocurcumin (HHC), a major metabolite of curcumin, has been reported to have protective effects against ischemic and reperfusion damage. The goal of the present research was to examine whether HHC could alleviate brain damage and ameliorate functional outcomes by diminishing the blood-brain barrier (BBB) damage that follows cerebral ischemia/reperfusion.
METHODS
METHODS
Middle cerebral artery occlusion was induced for 2 h in rats followed by reperfusion. The rats were divided into three groups: sham-operated, vehicle-treated, and HHC-treated groups. At the onset of reperfusion, the rats were immediately intraperitoneally injected with 40 mg/kg HHC. At 48 h after reperfusion, the rats were evaluated for neurological deficits and TTC staining. At 24 h and 48 h after reperfusion, animals were sacrificed, and their brains were extracted.
RESULTS
RESULTS
Treatment with HHC reduced neurological scores, infarct volume, morphological changes, Evans blue leakage and immunoglobulin G extravasation. Moreover, HHC treatment reduced BBB damage and neutrophil infiltration, downregulated myeloperoxidase, ICAM-1, and VCAM-1, upregulated tight junction proteins (TJPs), and reduced aquaporin 4 expression and brain water content.
CONCLUSION
CONCLUSIONS
These results revealed that HHC treatment preserved the BBB from cerebral ischemia/reperfusion injury by regulating TJPs, attenuating neutrophil infiltration, and reducing brain edema formation.
Identifiants
pubmed: 32048258
doi: 10.1007/s43440-019-00050-9
pii: 10.1007/s43440-019-00050-9
doi:
Substances chimiques
Aquaporin 4
0
Zonula Occludens-1 Protein
0
hexahydrocurcumin
0
Curcumin
IT942ZTH98
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
659-671Références
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