兰州大学机构库 >生命科学学院
枸杞叶总黄酮对小鼠脑缺血再灌注的保护作用
Alternative TitleNeuroprotective Effect of Total Flavonoids from Lycium barbarum Leaves against Cerebral Ischemia/Reperfusion Injury in Mice
徐少清
Thesis Advisor王建林
2016-05-19
Degree Grantor兰州大学
Place of Conferral兰州
Degree Name硕士
Keyword枸杞叶总黄酮 脑缺血再灌注 超氧化物歧化酶 丙二醛 Na+-K+-ATP酶 Ca2+-ATP酶
Abstract目的:通过建立小鼠脑缺血再灌注模型,探究枸杞叶总黄酮对小鼠脑缺血再灌注的保护作用,并从其抗氧化活性和对ATP酶活性影响方面探讨可能机制。 方法:小鼠随机分为6个小组。给药十四天,结扎双侧颈总动脉, 24小时后处死,取脑称重,计算脑指数和脑含水量。通过试剂盒检测小鼠脑组织中SOD活性、MDA含量及Na+-K+-ATP 酶和Ca2+-ATP酶的活性。通过HE染色观察大脑皮质及海马CA1区的神经元形态学变化。 结果: 1.在脑缺血再灌注模型中,高剂量的枸杞叶总黄酮能够有效降低小鼠的脑指数和脑含水量。 2.高剂量的枸杞叶总黄酮预处理后能显著减轻大脑的脂质过氧化程度,小鼠脑组织内的SOD活性明显提高,MDA的含量水平降低。 3.高剂量的枸杞叶总黄酮预处理后能显著抑制Na+-K+-ATP酶、Ca2+-ATP酶活性下降。 4.取小鼠脑组织进行HE染色发现模型组的小鼠大脑皮质及海马CA1区神经元有明显的损害,可观察到细胞核浓缩、核消失、神经元缺失等现象,正常的神经元数目减少。枸杞叶总黄酮预处理后则明显减轻了大脑皮质及海马CA1区神经元的损伤情况。 结论:枸杞叶总黄酮对于脑缺血具有保护作用,能够有效减轻脑缺血再灌注所引起的神经元损伤。其脑缺血的保护作用机制可能与提高机体抗氧化应激水平、保护脑组织ATP酶活性和改善离子转运有关。
Other AbstractAim: To observe neuroprotective effect of total flavonoids from Lycium barbarum leaves against cerebral ischemia/reperfusion ingury in mice and investigate its relating mechnisms from antioxidant activity and affect atpase activity. Method: 60 male kunming mice (postnatal 2months) were randomly divided into six groups, After transient cerebral global ischemia for 15minutes and 24hours reperfusion period, the mice were deeply anesthetized and decapitated. Brains were quickly removed to calculated brain index, and then bake to constant weight in 110℃ for calculating the brain water content. SOD activity, the level of MDA, Na+-K+-ATPase and Ca2+-ATPase were detected by kits. Morphological changes in the cerebral cortex and hippocampus CA1 area were observed by HE staining. Results: 1. Effect of total flavonoids from Lycium barbarum leaves on brain index and brain water content in ischemia/reperfusion mice was that high dose of total flavonoids extracts can effectively reduce the mice brain index and cerebral water content in ischemia/reperfusion mice(compared with model group). 2. Effect of total flavonoids from Lycium barbarum leaves on SOD activity and MDA level in ischemia/reperfusion mice was that the activity of SOD and the level of MDA were 110±3.9Uml and 6.1±0.4nmol/ml in sham-operated group, respectively. Ischemia/reperfusion group resulted in a significant decrease in SOD activity(down to 99.7±4.1Uml, compared with sham-operated group) and marked increase in MDA level(up to 9.9±0.9 nmol/ml, compared with sham-operated group). High dose of total flavonoids extract pretreatment can significantly reduce the peroxidative degree of lipid, obviously improve the SOD activity (compared with model group, P < 0.05, n = 10), and reduce the MDA level in the brain (compared with model group, P < 0.05, n = 10). 3. Effect of total flavonoids from Lycium barbarum leaves on the level of Na+-K+-ATPase and Ca2+-ATPase in ischemia/reperfusion mice was that the activity of Na+-K+-ATPase and Ca2+-ATPase were 1.77±0.50μmol/mgprot/h and 1.85±0.47μmol/mgprot/h in sham-operated group, respectively. Ischemia/reperfusion group resulted in a significant decrease in the activity of Na+-K+-ATPase (up to 1.07±0.30μmol/mgprot/h, compared with sham-operated group) and marked decrease in the activity of Ca2+-ATPase (up to 1.16±0.27μmol/mgprot/h, compared with sham- operated group). High dose of total flavonoids extract pretreatment can significantly inhibite the activ...
URL查看原文
Language中文
Document Type学位论文
Identifierhttps://ir.lzu.edu.cn/handle/262010/221315
Collection生命科学学院
Recommended Citation
GB/T 7714
徐少清. 枸杞叶总黄酮对小鼠脑缺血再灌注的保护作用[D]. 兰州. 兰州大学,2016.
Files in This Item:
There are no files associated with this item.
Related Services
Recommend this item
Bookmark
Usage statistics
Export to Endnote
Altmetrics Score
Google Scholar
Similar articles in Google Scholar
[徐少清]'s Articles
Baidu academic
Similar articles in Baidu academic
[徐少清]'s Articles
Bing Scholar
Similar articles in Bing Scholar
[徐少清]'s Articles
Terms of Use
No data!
Social Bookmark/Share
No comment.
Items in the repository are protected by copyright, with all rights reserved, unless otherwise indicated.