Cornel Iridoid Glycoside Inhibits Inflammation and Apoptosis in Brains of Rats with Focal Cerebral Ischemia

被引：50

作者：

Ya, Bai-liu ^{[1
]}

Li, Chun-yang ^{[2
]}

Zhang, Lan ^{[1
]}

Wang, Wen ^{[1
]}

Li, Lin ^{[1
]}

机构：

[1] Capital Med Univ, Xuanwu Hosp, Dept Pharmacol, Key Lab Neurodegenerat Dis,Minist Educ, Beijing 100053, Peoples R China

[2] Inner Mongolia Med Coll, Dept Neurol, Affiliated Hosp, Hohhot 010059, Inner Mongolia, Peoples R China

来源：

NEUROCHEMICAL RESEARCH | 2010年 / 35卷 / 05期

基金：

中国国家自然科学基金;

关键词：

Cornus; Iridoid glycosides; Focal cerebral ischemia; Cerebral infarction; Neuroinflammation; Apoptosis; ARTERY OCCLUSION; DNA FRAGMENTATION; FRUCTUS; INTERLEUKIN-1; INFARCTION; RESPONSES; STROKE;

D O I：

10.1007/s11064-010-0134-2

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

070307 [化学生物学]; 071010 [生物化学与分子生物学];

摘要：

The capacity of cornel iridoid glycoside (CIG) to suppress the manifestations of ischemic stroke was investigated. CIG was administered to rats by the intragastric route once daily for 7 days. Focal cerebral ischemia was induced by 2 h of middle cerebral artery occlusion followed by 24 h of reperfusion. In non-treated rats large infarct areas were observed within 24 h of reperfusion. Examination of the ischemic cerebral cortex revealed microglia and astrocyte activation, increased interleukin-1 beta (IL-1 beta) and tumor necrosis factor-alpha (TNF-alpha) concentrations, increased DNA fragmentation in the ischemia penumbra, elevated Bax expression, increased caspase-3 cleavage, and decreased Bcl-2 expression. Pretreatment with CIG decreased the infarct area, DNA fragmentation, IL-1 beta and TNF-alpha concentrations, microglia and astrocyte activation, Bax expression, and caspase-3 cleavage while increasing Bcl-2 expression. CIG exerts anti-neuroinflammatory and anti-apoptotic effects which should prove beneficial for prevention or treatment of stroke.

引用

页码：773 / 781

页数：9

共 37 条

[1]

Anti-apoptotic and neuroprotective effects of edaravone following transient focal ischemia in rats [J].