| 霍奇帆,郭建伟,蒋延安,张世平,赵 静.右美托咪定通过抑制线粒体凋亡水平缓解大鼠脑缺血后记忆障碍的实验研究[J].,2021,(22):4234-4237 |
| 右美托咪定通过抑制线粒体凋亡水平缓解大鼠脑缺血后记忆障碍的实验研究 |
| Experimental Research on Dexmedetomidine Alleviates the Rat's Memory with Cerebral Ischemia by Inhibiting Mitochondrial Apoptosis |
| 投稿时间：2021-04-04 修订日期：2021-04-27 |
| DOI：10.13241/j.cnki.pmb.2021.22.007 |
| 中文关键词: 脑缺血 记忆障碍 右美托咪定 线粒体 大鼠 |
| 英文关键词: Cerebral ischemia Memory impairment Dexmedeidine Mitochondri Rats |
| 基金项目:陕西省自然科学基础研究项目（2018JM-661） |
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| 摘要 目的：探右美托咪定缓解缺血性脑损伤记忆障碍大鼠记忆功能的作用机制。方法：选择雄性SD大鼠36只，随机分为三组，分别为：假手术组（12只）、缺血性脑损伤模型组（12只）、右美托咪定组（12只），除假手术组外其余动物均采用双侧颈动脉结扎术建立慢性脑缺血模型。假手术组和模型组给予生理盐水静注，右美托咪定组给予右美托咪定0.5 μg /kg，静注，均在15 min内滴完。比较大鼠给药前和给药后4 w的记忆情况以及线粒体凋亡因子Bcl-2、Cleaved Caspase-3、Caspase-9的表达水平。结果：（1）与假手术组相比，模型组和右美托咪定组大鼠逃逸潜伏期明显增高（P＜0.05），右美托咪定组逃逸潜伏期与模型组相比有显著降低（P＜0.05）；与假手术组相比，模型组和右美托咪定组大鼠游泳路程明显延长（P＜0.05），右美托咪定组游泳路程与模型组相比有显著降低（P＜0.05）；（2）与假手术组相比，模型组和右美托咪定组大鼠海马区部分凋亡因子Bcl-2，Cleaved Caspase-9，Cleaved Caspase-3的蛋白表达均有明显提升（P＜0.05）；与模型组相比，右美托咪定组在给药4 w后上述蛋白的表达有明显降低（P＜0.05）。结论：右美托咪定对脑缺血记忆障碍大鼠的记忆功能有显著改善作用，其作用机制可能与抑制线粒体凋亡水平有关，具体信号通路还有待进一步探索。 |
| 英文摘要: |
| ABSTRACT Objective: To explore the mechanism of dexmedeidine in relieving memory impairment in ischemic brain injury rats. Methods: The 36 male SD rats were randomly divided into three groups, respectively is: the sham operation group(12 rats), ischemic brain injury model group(12 rats) and dexmedetomidine group(12 rats), in addition to control the rest of the animal adopt bilateral carotid ligation were chronic cerebral ischemia model control group and model group was given saline static note, dexmedetomidine group was given the dexmedetomidine 0.5 μg/kg, static note, drip off within 15 min. Compared the rats' memory before and within 4 w after administration, as well as the expression levels of mitochondrial apoptotic factors Bcl-2, Cleaved caspase-3, and caspase-9. Results: (1) Compared with the sham operation group, the escape latency of rats in the model group and dexmedetomidine group was significantly increased(P＜0.05), and the escape latency of the dexmedetomidine group was significantly lower than that of the model group(P＜0.05); Compared with the sham operation group, the swimming distance of rats in the model group and the dexmedetomidine group was significantly longer(P＜0.05), and the swimming distance of the dexmedetomidine group was significantly reduced compared with the model group(P＜0.05). (2) Compared with the sham operation group, the protein expression of some apoptosis factors Bcl-2, Cleaved Caspase-9 and Cleaved Caspase-3 in the hippocampus of the model group and dexmedetomidine group were significantly increased(P＜0.05); Compared with the model group, the expression of the above-mentioned protein in the dexmedetomidine group was significantly reduced after 4 weeks of administration(P＜0.05). Conclusion: Dexmedeidine can significantly improve the memory function of rats with cerebral ischemia and memory dysfunction, and its mechanism may be related to the inhibition of mitochondrial apoptosis. The specific signaling pathway remains to be further explored. |
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