文章摘要
Nrf2对缺血再灌注损伤中线粒体分裂的调控<sub><sup>*</sup></sub>
The Regulation of Nrf2 on mitochondrial division in ischemia-reperfusion injury
投稿时间:2019-02-27  修订日期:2019-02-27
DOI:
中文关键词: Nrf2  线粒体分裂  Drp1  脑缺血再灌注损伤
英文关键词: Nrf2  Mitochondrial fission  Drp1  Cerebral ischemia reperfusion injury
基金项目:国家自然科学(81771415);,国家自然科学基金项目(面上项目,重点项目,重大项目)
作者单位E-mail
黄林 青岛大学 青岛 中国 794209186@qq.com 
刘茂东 青岛大学附属医院 青岛 中国  
李瑜 青岛大学附属医院 青岛 中国  
王亚楠 青岛大学 青岛 中国  
王士雷 青岛大学附属医院 青岛 中国  
 青岛大学 青岛 中国
青岛大学附属医院 青岛 中国 
 
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中文摘要:
      目的:通过建立体外脑缺血再灌注损伤损伤的细胞模型,研究Nrf2信号通路与线粒体分裂是否存在调控关系。方法:通过利用三气培养箱建立氧糖剥夺再恢复的细胞系模型。CCK8法检测细胞的存活率,Western blot法测目标Nrf2、Drp1蛋白表达量,电镜观察细胞内线粒体形态。结果: 选定SH-SY5Y细胞作为目标细胞系,并成功建立细胞OGD/R模型。Western blot测得OGD/R+tBHQ组的Nrf2蛋白表达较OGD/R组增加且Drp1蛋白的表达相应减少,而OGD/R+Brusatol组Nrf2蛋白表达较OGD/R组减少且Drp1蛋白的表达相应增多(p<0.05);电镜观察结果显示OGD/R+tBHQ组线粒体分裂较OGD/R组相应减轻,而OGD/R+Brusatol组加重。结论:Nrf2信号通路对线粒体分裂有调控作用,可能机制是经由Drp1蛋白起作用。
英文摘要:
      ABSTRACT Objective: To investigate the relationship between Nrf2 signaling pathway and mitochondrial division in cerebral ischemia-reperfusion injury in. Methods: A three-gas incubator was used to form a cell line model of oxygen glucose deprivation/restoration. The survival rate of the cells was detected by CCK8 method. The expressions of protein Nrf2 and Drp1 protein were detected by Western blot, and the mitochondrial morphology was observed by electron microscope. Results: SH-SY5Y cells were selected as the target cell line, and the cell OGD/R model was successfully established. The expression of Nrf2 protein in OGD/R+tBHQ group was increased compared with it in OGD/R group and the expression of Drp1 protein was decreased, detected by Western blot. The expression of Nrf2 protein in OGD/R+Brusatol group was raised compared with that in OGD/R group and the expression of Drp1 protein was inclined(p<0.05). The results by electron microscopy showed that the mitochondrial division in the OGD/R+tBHQ group was reduced compared with the OGD/R group, while the OGD/R+Brusatol group was ag gravated. Conclusion: The Nrf2 signaling pathway regulates mitochondrial division, and the possible mechanism is via Drp1 protein.
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