| 王 瑜,周凌雪,王天龙,赵 磊,李 丽.局部脑缺血再灌注损伤小鼠脑组织TMEM166的表达及其与脑细胞凋亡的关系[J].,2018,(12):2201-2204 |
| 局部脑缺血再灌注损伤小鼠脑组织TMEM166的表达及其与脑细胞凋亡的关系 |
| Effect of TMEM166 on Neuron Apoptosis in Mice after Focal Brain Ischemia Reperfusion Injury |
| 投稿时间：2017-12-31 修订日期：2018-01-26 |
| DOI：10.13241/j.cnki.pmb.2018.12.001 |
| 中文关键词: TMEM166 脑缺血再灌注 凋亡 |
| 英文关键词: TMEM166 Cerebral ischemia/reperfusion Apoptosis |
| 基金项目:国家自然科学基金项目(81500996)；北京市215高层次卫生技术人才学术带头人资助项目（008-0027）；北京市医院管理局“登峰计划”专项（DFL20150802） |
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| 中文摘要: |
| 摘要 目的：观察跨膜蛋白166 (Transmembrane protein 166，TMEM166)基因在小鼠局部脑缺血再灌注损伤(MCAO)后的表达改变及其对脑细胞凋亡的影响。方法：C57/BL6J雄性小鼠50只，体重22-28 g，采用线栓法制作MCAO模型，缺血后动物随机分为再灌注6、12、24、48 h 组。采用免疫组化染色的方法观察缺血侧大脑TMEM166、Caspase 3的阳性细胞数目，TUNEL标记法检测细胞凋亡情况，Western blot检测不同再灌注时间点TMEM166、Caspase 3蛋白水平的表达。结果：缺血侧TMEM166的表达随着再灌注时间的延长而增加，24 h达到高峰，48 h后逐渐下降；再灌注6 h后Caspase 3观察到有表达，同样随着再灌注时间而升高，24 h达到高峰。缺血侧细胞凋亡数量变化趋势与TMEM166基本一致，对侧大脑半球上述指标无明显变化。结论：小鼠局部脑缺血再灌注损伤时伴有TMEM166的表达升高，可能通过激活Caspase 3引起脑细胞凋亡。 |
| 英文摘要: |
| ABSTRACT Objective: To investigate the expression of TMEM166(Transmembrane protein 166) and its effect on neuron apoptosis in mice after middle cerebral artery occlusion (MCAO). Methods: Fifty C57/BL6J male mice weighing 22-28 g were randomly divided into five groups according to different reperfusion time points at 6, 12, 24 and 48 h, respectively. TMEM166 and Caspase 3 were measured by immunochemistry staining. TUNEL staining was conducted to observe the neuron apoptosis. Protein levels of TMEM166 and Caspase 3 were detected by Western blot. Results: TMEM166 was induced in mice after cerebral ischemia reperfusion injury, and it has peaked at 24 h after injury in the ischemia hemisphere. Cleaved Caspase 3 began to increase at 6 h following MCAO, which then kept going up over time and also reached the highest level at 24 h after ischemia insult. Changing pattern of TMEM166 level in this process was consis- tent with the changes of TUNEL positive cell numbers. No changes of TMEM166 was found in the contralateral hemisphere. Conclusion: TMEM166 was induced after MCAO, and it could lead to cell apoptosis by activating Caspase 3. |
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