Effects of icariside II on brain tissue oxidative stress and Nrf2/HO-1 expression in rats with cerebral ischemia-reperfusion injury1.

IF 1.3 4区 医学 Q3 SURGERY Acta cirurgica brasileira Pub Date : 2019-02-28 DOI:10.1590/s0102-8650201900208
Yan Li, Fanjun Meng
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引用次数: 14

Abstract

Purpose: To investigate the effects of icariside II on brain tissue oxidative stress and Nrf2/HO-1 expression in rats with cerebral ischemia-reperfusion injury (CIRI).

Methods: One hundred SD rats were randomly divided into sham-operated, model, and 5, 10 and 20 mg/kg icariside II groups, 20 rats in each group. The middle cerebral artery occlusion model (ischemia for 2 h followed by reperfusion for 24 h) was established in the later 4 groups. In later 3 groups, at reperfusion beginning, the rats were intragastrically administrated with 5, 10 and 20 mg/kg icariside II, respectively. After 24 h of reperfusion, the neurological severity score, cerebral water content and cerebral infarction volume, brain tissue oxidative stress indexes and Nrf2 and HO-1 protein expressions were determined.

Results: Compared with model group, in 20 mg/kg icariside II group the neurological severity score, cerebral water content and cerebral infarction volume, brain tissue ROS content and MDA level were significantly decreased (P<0.05), and the brain tissue SOD, GSH-Px and catalase levels and Nrf2 and HO-1 protein levels were significantly increased (P<0.05).

Conclusion: Icariside II can alleviate the CIRI in rats through reducing brain tissue oxidative stress and improving Nrf2/HO-1 expression.

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红豆苷II对脑缺血再灌注损伤大鼠脑组织氧化应激及Nrf2/HO-1表达的影响
目的:探讨红豆苷II对脑缺血再灌注损伤大鼠脑组织氧化应激及Nrf2/HO-1表达的影响。方法:将100只SD大鼠随机分为假手术组、模型组和5、10、20 mg/kg甘蓝素组,每组20只。后4组均建立大脑中动脉闭塞模型(缺血2 h再灌注24 h)。后3组大鼠在再灌注开始时,分别灌胃5、10、20 mg/kg的甘薯苷II。再灌注24 h后,测定大鼠神经系统严重程度评分、脑含水量、脑梗死体积、脑组织氧化应激指标及Nrf2、HO-1蛋白表达。结果:与模型组比较,20 mg/kg icariside II组大鼠神经系统严重程度评分、脑水含量、脑梗死体积、脑组织ROS含量及MDA水平均显著降低(p)。结论:icariside II可通过降低脑组织氧化应激、提高Nrf2/HO-1表达来减轻大鼠CIRI。
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来源期刊
CiteScore
1.90
自引率
9.10%
发文量
60
审稿时长
3-8 weeks
期刊介绍: Information not localized
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