Coumestrol treatment prevents Na+, K+-ATPase inhibition and affords histological neuroprotection to male rats receiving cerebral global ischemia
Coumestrol treatment prevents Na+, K+-ATPase inhibition and affords histological neuroprotection to male rats receiving cerebral global ischemia
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DOI：
10.1179/1743132813y.0000000286
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发表时间：
2014-03-01
影响因子：
1.9
通讯作者：
Netto, Carlos Alexandre
中科院分区：
文献类型：
--
作者：
Castro, Cibele Canal;Pagnussat, Aline S.;Netto, Carlos Alexandre
目的：在一种男性受试者的全脑缺血模型中，我们研究了香豆素(Coumestrol)的神经保护作用的可能机制。香豆素是一种有效的异黄酮类化合物，具有抗氧化活性和雌激素受体ER-α和ER-β的结合亲和力，与17β-雌二醇相当。方法：Wistar大鼠进行全脑缺血(10分钟)或假手术，在缺血前1小时或再灌流后0、3、6或24小时，脑室一次性注入20 MU的库美斯特罗或赋形剂。结果：数据分析显示，在7天、6天或24小时，CA1区神经元广泛死亡在脑缺血后1小时和24小时，Na+，K+-ATPase活性显著降低，两种损伤均可被给予香豆素缓解。结论：香豆酚在所有给药时间段均能有效地防止神经元丢失，并能恢复Na+，K+-ATPase活性，对预防和治疗男性脑缺血具有潜在的作用。
Objective: In this study, we investigated the possible mechanisms underlying the neuroprotective effects of coumestrol, a potent isoflavonoid with antioxidant activities and binding affinities for both estrogen receptors (ER) ER-alpha and ER-beta that are comparable to those of 17beta-estradiol, in a model of global ischemia in male subjects.Methods: Wistar rats underwent global ischemia (10 minutes) or sham surgery and received a single intracerebroventricular (icv) infusion of 20 mu g of coumestrol or vehicle 1 hour before ischemia or 0, 3, 6, or 24 hours after reperfusion.Results: The data analysis revealed an extensive neuronal death in the CA1 hippocampal subfield at 7 days, and a significant decrease in the Na+, K+-ATPase activity at 1 and 24 hours after ischemia, and both injuries were attenuated by coumestrol administration.Conclusions: Coumestrol treatment was effective in preventing neuronal loss in all times of administration as well as able to rescue the Na+, K+ -ATPase activity, suggesting its potential benefits for either prevention or therapeutics use against cerebral ischemia in males.