The protective role of verbenalin in rat model of focal cerebral ischemia reperfusion

被引:17
作者
Cao, Lihua [1 ]
Miao, Mingsan [1 ]
Qiao, Jingyi [1 ]
Bai, Ming [1 ]
Li, Ruiqi [1 ]
机构
[1] Henan Univ TCM, Dept Pharmacol, Zhengzhou 450046, Henan, Peoples R China
关键词
Verbenalin; Focal cerebral ischemia-reperfusion; Apoptosis; INJURY; CASPASE-3; BCL-2;
D O I
10.1016/j.sjbs.2017.10.005
中图分类号
Q [生物科学];
学科分类号
07 ; 0710 ; 09 ;
摘要
To investigate the protective mechanism of verbenalin on cerebral ischemia-reperfusion injury. Middle cerebral artery occlusion in the left hemisphere was induced in rats by filament insertion, and rat model of focal cerebral ischemia-reperfusion was established. The high, medium and low dose of verbenalin groups were injected in the tail vein of corresponding drugs 10 min before reperfusion, and submitted for 22 h of reperfusion after the operation. Mortality rate was then calculated, and neurological deficits of rats were scored. The serum of rats was got to determine the S-100 beta protein level, and the brain tissue was removed to determine the levels of Bax, Bcl-2, Caspase-3 and ATPase. TTC staining was performed on the brain tissue to calculate the percentage of cerebral infarct size. Changes in brain tissue morphology were observed. Rat model of focal cerebral ischemia-reperfusion was successfully replicated. In groups that have taken different doses of verbenalin, the mortality rate, neurological deficit score and the percentage of cerebral infarction size were significantly reduced, and the levels of Bax, Caspase-3, S-100 beta level of the serum in the brain tissue were also significantly reduced. Increases in the levels of Bcl-2 and ATPase in brain tissue and improvement of pathological damage of hippocampus and cortex were observed. Verbenalin can inhibit the expression of apoptosis genes, promote the expression of antiapoptosis genes, improve brain microcirculation and energy metabolism, hence reducing cerebral ischemia-reperfusion injury. (C) 2017 Production and hosting by Elsevier B.V.
引用
收藏
页码:1170 / 1177
页数:8
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