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作 者:周立田[1] 王汉东[1] 金伟[1] 乔梁[1] 唐科[1] 茅磊[1] 王笑亮[1]
机构地区:[1]南京大学医学院临床学院南京(南京军区南京总医院)神经外科,医学硕士研究生210002
出 处:《医学研究生学报》2010年第5期470-473,共4页Journal of Medical Postgraduates
基 金:江苏省医学重点学科基金(X4200722);南京军区科技创新课题基金(072029)
摘 要:目的 Nrf2在脑外伤后脑保护可能具有重要的作用,其作用机制尚不明确;文中研究Nrf2在脑外伤后继发性脑损伤中对神经细胞钙离子稳态及凋亡的影响并探讨其可能的作用机制。方法用自由落体致伤的方法制作小鼠脑外伤模型,分为Nrf2(-/-)外伤组、Nrf2(+/+)外伤组、Nrf2(-/-)对照组、Nrf2(+/+)对照组;分别检测实验性外伤24 h后神经细胞内游离钙离子浓度和神经细胞凋亡指数。结果外伤组脑组织神经细胞内游离钙离子浓度、神经细胞凋亡指数显著高于对照组(P<0.01);与Nrf2(+/+)外伤组相比,Nrf2(-/-)外伤组改变更显著(P<0.05);对照组之间无明显差异(P>0.05)。结论 Nrf2通路是脑外伤后保持神经细胞钙离子稳态和减轻神经细胞凋亡的保护性通路。Objective Nrf2 plays an important role in traumatic brain injury,whose mechanism is unclear.The purpose of this study is to explore the effects and mechanism of Nrf2 on intracellular free Ca2+ concentration and apoptosis in mice brain after experimental traumatic brain injury(TBI).Methods The brain injury of the mice was induced with a free dropping impact.Forty ICR mice were randomly divided into four groups:injured Nrf2(-/-),injured Nrf2(+/+),sham Nrf2(-/-) and sham Nrf2(+/+);The concentration of intracellular free Ca2+and apoptosis index were evaluated 24 h after TBI.Results At 24 h after TBI,increased intracellular free Ca2+concentration and apoptotic index were found in both injured Nrf2(+/+)and Nrf2(-/-) mice compared with their respective sham-operated mice(P0.01).However,the pathological change was more severe in Nrf2(-/-) mice compared with Nrf2(+/+) mice(P0.05).Conclusion Nrf2 maintains the neuronal calcium homeostasis and mitigates the neuronal apoptosis,which is a protective pathway after TBI.
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