Baicalin attenuates in vivo and in vitro hyperglycemia-exacerbated ischemia/reperfusion injury by regulating mitochondrial function in a manner dependent on AMPK.
Eur J Pharmacol
; 815: 118-126, 2017 Nov 15.
Article
in En
| MEDLINE
| ID: mdl-28743390
ABSTRACT
Cerebral ischemia/reperfusion (I/R) is a lethal and disabling disease. Studies have suggested that hyperglycemia is a risk factor for cerebral I/R. Baicalin is a natural bioactive flavonoid extracted from Scutellaria baicalensis Georgi with neuroprotective activity. In the present study, we investigated the effects of baicalin on hyperglycemia-exacerbated cerebral I/R injury. Streptozotocin (STZ) injection aggravated the brain damage induced by middle cerebral artery occlusion (MCAO) surgery, while baicalin administration reduced blood glucose, relieved neurological deficit and decreased infarct volume. In vitro, Oxygen-glucose deprivation/ reperfusion (OGD/REP) induced inordinate reactive oxygen species (ROS) production and mitochondrial dynamic impairments were markedly increased under high glucose (HG) condition. Baicalin treatment in PC12 cells inhibited dynamin-related protein 1 (Drp-1) expression, decreased mitochondrial fission, promoted mitofusin-2 (MFN2) generation, increased Drp-1 Ser637 phosphorylation, and elevated mitochondrial membrane potential (Δψm) via the suppression of ROS production. However, AMPKα1 knockdown abolished the protective effects of baicalin. Baicalin also suppressed cell apoptosis and enhanced mitophagy. These results suggested that baicalin protected against hyperglycemia aggravated I/R injury by regulating mitochondrial functions in a manner dependent on AMPK.
Key words
Full text:
1
Collection:
01-internacional
Database:
MEDLINE
Main subject:
Flavonoids
/
Reperfusion Injury
/
Neuroprotective Agents
/
AMP-Activated Protein Kinases
/
Hyperglycemia
/
Mitochondria
Type of study:
Risk_factors_studies
Limits:
Animals
Language:
En
Journal:
Eur J Pharmacol
Year:
2017
Document type:
Article
Affiliation country:
China