缺血
细胞凋亡
再灌注损伤
黄芪甲苷
下调和上调
医学
药理学
蛋白激酶A
内分泌学
麻醉
内科学
脑梗塞
化学
激酶
生物化学
高效液相色谱法
基因
色谱法
作者
Yu Li,Yuting Wang,Jingxue Tang,Zhaorui Shu,Xian Han
出处
期刊:Neuroreport
[Ovid Technologies (Wolters Kluwer)]
日期:2022-09-07
卷期号:33 (15): 656-662
被引量:3
标识
DOI:10.1097/wnr.0000000000001831
摘要
To determine the effects of astragaloside IV on cerebral ischemic-reperfusion injury in rats and to explore underlying mechanisms of brain protection.Sixty Sprague-Dawley rats were randomized into four groups: Sham, cerebral ischemia-reperfusion (I/R group), I/R+astragaloside IV (I/R+AST-IV group) and I/R+astragaloside IV+PKA kinase inhibitor H-89 (I/R+AST-IV+H-89 group). All I/R rats were subjected to 2 h cerebral ischemia, followed by 24 h reperfusion and scored for neurobehavior. Cerebral infarct volume, pathomorphological changes and brain apoptosis, in addition to changes in expression of Cx36, PKA, Bax and Bcl-2 proteins, were assessed.Astragaloside IV treatment reduced neurobehavioral score and percentage volume of cerebral infarct, reducing pathomorphological injury and brain apoptosis. Expressions of Cx36 and PKA protein were increased and the Bax/Bcl-2 ratio decreased. All astragaloside IV effects were reversed by the PKA inhibitor and H-89.Astragaloside IV attenuated cerebral I/R injury in rats by increasing Cx36 and PKA protein expression and reducing the Bax/Bcl-2 ratio.
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