| 曾琳，谢明，武衡，尹凯.17β-雌二醇共价衍生物（E2-BSA）对脑缺血再灌注大鼠神经元早期损伤的保护作用.[J].中南医学科学杂志.,2011,39(5):518-521. |
| 17β-雌二醇共价衍生物（E2-BSA）对脑缺血再灌注大鼠神经元早期损伤的保护作用 |
| Protective Effects of 17β-estradiol Conjugate (E2-BSA) on Cerebral Ischemia Reperfusion-induced Neurocyte Injury |
| 投稿时间：2011-04-13 |
| DOI： |
| 中文关键词: 17β-雌二醇共价衍生物 胱天蛋白酶3 神经保护 脑缺血再灌注 |
| 英文关键词:17β-estradiol conjugate neuroprotection caspase-3 cerebral ischemic-reperfusion |
| 基金项目:湖南省卫生厅项目（B2007092）. |
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| 中文摘要: |
| 目的研究17β-雌二醇衍生物（E2-BSA）对大鼠脑缺血再灌注损伤模型神经细胞早期损伤的保护作用及其对caspase-3蛋白表达的影响。方法将50只去势SD大鼠随机分为5组（n=10）：假手术组（SH）、脑缺血再灌注+生理盐水组(IRI)和三种浓度（5、10、15 μmol/L）E2-BSA处理组。HE染色观察大鼠侧脑皮层神经元损伤的状况，Western-blot检测E2-BSA对Caspase 3蛋白表达的影响。结果HE染色显示，E2-BSA对缺血再灌注引起的侧脑皮层神经损伤具有保护作用，其中10 μmol/L E2-BSA处理组大鼠侧脑皮层神经细胞损伤较轻。Western blot显示，脑缺血再灌注损伤组的caspase-3蛋白表达明显增多（P<0.05）；而E2-BSA治疗后，caspase-3蛋白表达明显减少（P<0.05），其中10 μmol/L E2-BSA处理组caspase-3蛋白表达量最少。结论E2-BSA对脑缺血再灌注损伤神经元具有保护作用，该效应可能与抑制Caspase-3活性有关。 |
| 英文摘要: |
| ObjectiveTo observe the effect of 17β-estradiol conjugate (E2-BSA) on expression of caspase 3.Methods50 ovariectomy SD rats were randomly divided into 5 groups,according to cerebral ischemia reperfusion-induced neurocyte injury and the activation,sham operation group(SH),Reperfusion+ physiological saline group(IRI)and 3 groups treated with different concentration(5，10，15 μmol/L)of E2-BSA.Hematoxylin-eosin(HE)staining were conducted to test the neuronal injury induced by ischemic-reperfusion;Western blot were conducted to determine the expression of caspase 3.ResultsE2-BSA had neuroprotective effects on the neuronal injury induced by ischemic-reperfusion,and 10 μmol/L was the best pre-protective concentration.Western blot results showed that the expression of caspase 3 in the reperfusion group was significantly increased(P<0.05)；However，the expression of caspase 3 in the groups treated with E2-BSA were lower than that of the reperfusion group（P<0.05），especially in 10 μmol/L E2-BSA-treated group.ConclusionsE2-BSA could play a neuroprotective role in the neurocyte injury induced by the cerebral ischemia reperfusion via suppressing the activity of Caspase-3. |
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