| 韩 东,武 卿,蒋倩蓉,胡书群,许 铁.NSC23766对海马CA1区神经元缺血性损伤的保护机制[J].,2017,17(35):6823-6827 |
| NSC23766对海马CA1区神经元缺血性损伤的保护机制 |
| Neuroprotective Mechanisms NSC23766 against Global Cerebral Ischemia in Rat Hippocampal CA1 Region |
| 投稿时间：2017-07-23 修订日期：2017-08-18 |
| DOI：10.13241/j.cnki.pmb.2017.35.006 |
| 中文关键词: 缺血再灌注 Rac1 NSC23766 c-Jun ATF2 |
| 英文关键词: Ischemia-reperfusion Rac1 NSC23766 c-Jun ATF2 |
| 基金项目:江苏省自然科学基金面上研究项目（BK20161153）；徐州医学院院长基金项目（2012KJZ16） |
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| 中文摘要: |
| 摘要 目的：探讨抑制Ras相关的C3肉毒素底物1 （ras-related C3 botulinum toxin substrate 1, Rac1）活化对海马CA1区神经元缺血性损伤产生保护作用的机制。方法：采用大鼠大脑四动脉结扎建立全脑缺血模型，SD雄性大鼠按照随机数字法被分为假手术（Sham）组，缺血再灌注（ischemia / reperfusion，I/R）组，溶剂对照（Vehicle）组，NSC23766预处理（NSC）组。Vehicle组、NSC组分别在缺血前30 min侧脑室注射0.9%的生理盐水（5 μL）和Rac1特异性抑制剂NSC23766（25 μg溶于5 μL 0.9%的生理盐水）。蛋白免疫印迹法检测海马CA1区c-Jun、活化转录因子-2 （activating transcription factor2, ATF2）、P-c-Jun、P-ATF2蛋白含量的变化。焦油紫染色法观察海马CA1区神经元的存活情况。结果：再灌注1d时，与I/R组相比，NSC组P-c-Jun、P-ATF2蛋白含量明显降低（P<0.05）；而c-Jun、ATF2蛋白含量没有明显变化；焦油紫结果显示，NSC组大鼠海马CA1区神经元死亡明显减少（P<0.05）。结论：NSC23766抑制Rac1活化对神经元缺血性损伤产生的保护作用可能与c-Jun、ATF2磷酸化水平降低有关。本研究的发现为临床治疗缺血性脑中风提供了新的靶点。 |
| 英文摘要: |
| ABSTRACT Objective: To explore the neuroprotection mechanisms of Inhibit the activation of ras-related C3 botulinum toxin sub- strate 1(Rac1) against global ischemia in rat Hippocampal CA1 Region. Methods: Using 4-vessel occlusion (4-VO) as brain ischemia model. The SD Male rats were randomly assigned into sham (sham) group, ischemia / reperfusion (I / R) group, Vehicle control group (Vehicle), and NSC23766 Pretreatment (NSC) group using a random number table. Vehicle group and NSC group were respectively in- jected 0.9% saline (5 μL) and Rac1 specific inhibitor NSC23766 (25 ug for 5 μL 0.9% saline) by intracerebroventricular to the rats 30 min before ischemia. The levels of c-Jun, activating transcription factor2（ATF2）, P-c-Jun and P-ATF2 proteins in hippocampal CA1 re- gion were detected by Western Blot and Cresyl violet staining was used to examine the survival of hippocampal CA1 pyramidal neurons. Results: After 1 day of reperfusion, Compared with I / R group, the content of P-c-Jun and P-ATF2 protein in NSC group was significantly lower than that in I / R group (P<0.05), but the content of c-Jun and ATF2 protein was not significantly Changes. Cresyl violet staining showed that the neuronal death of hippocampal CA1 regions of rats in the p38-I group was significantly decreased (P<0.05). Conclusion: Neuroprotective effect of NSC23766 inhibited Rac1 activation against ischemic brain injury may be associated with a decrease in phos- phorylation levels of c-Jun and ATF2 proteins. The findings of this study provide a new target for clinical treatment of ischemic stroke. |
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