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Oxymatrine Alleviates Hyperglycemic Cerebral Ischemia/Reperfusion Injury via Protecting Microvessel.

Authors :
Wang, Wen-Jun
Ma, Yan-Mei
He, Mao-Tao
Zhang, Deng-Hai
Wang, Rui
Jing, Li
Zhang, Jian-Zhong
Source :
Neurochemical Research. May2022, Vol. 47 Issue 5, p1369-1382. 14p.
Publication Year :
2022

Abstract

Hyperglycemia aggravates cerebral ischemia/reperfusion (I/R) injury via vascular injury. There is still a lack of effective pharmaceutical preparations for cerebral I/R injury under hyperglycemia. This study aimed to investigate the effects of oxymatrine (OMT) on hyperglycemia-exacerbated cerebral I/R injury in vitro and in vivo. The middle cerebral artery occlusion (MCAO) and reperfusion was established in the rats under hyperglycemia. Meanwhile, oxygen–glucose deprivation and reoxygenation (OGD/R) with high glucose was used as an in vitro model of hyperglycemic cerebral I/R injury. The results showed that the neurological deficit score, mortality, infarct volume and penumbra apoptosis in hyperglycemia group were significantly higher than those in normal glucose group. OMT pre-treated obviously reduced the degree of neurological deficit, mortality, infarct volume, improve cerebral blood flow after I/R in rats with hyperglycemia, and increase the survival rate of human brain microvascular endothelial cells (HBMECs) in high glucose and OGD/R group. OMT significantly improved the ultrastructure changes of endothelial cells, and maintain the migration and angiogenesis potency of HBMECs in high glucose and OGD/R group. OMT obviously alleviated the down-regulating CD31 and CD105 expression in cerebral microvessels caused by hyperglycemia. It is concluded that OMT treatment might alleviate cerebral I/R injury under hyperglycemia via protecting microvessels. [ABSTRACT FROM AUTHOR]

Details

Language :
English
ISSN :
03643190
Volume :
47
Issue :
5
Database :
Academic Search Index
Journal :
Neurochemical Research
Publication Type :
Academic Journal
Accession number :
156022846
Full Text :
https://doi.org/10.1007/s11064-022-03535-x