Dexmedetomidine (DEX) has neuroprotective effects and its efficacy was determined in propofol-treated pups. Postnatal day (P) 7 rats were exposed to propofol and DEX to investigate the induced apoptosis-related gene expression. Furthermore, synaptic structural changes at the cellular level were observed by electron microscopy. Induction of hippocampal long-term potentiation (LTP) of P30 rats and long-lasting performance of spatial discrimination at P30 and P60 were evaluated. After a single propofol exposure to P7 rats, DEX pretreatment effectively rescued the profound apoptosis seen in hippocampal neurocytes, and strongly reversed the aberrant expression levels of Bcl2-like 1 (BCL2L1), matrix metallopeptidase 9 (MMP-9) and cleaved caspase 3 (CC3), and sharply enhanced synaptic plasticity. However, there were no significant differences in escape latency or crossing times in a probe test. This was accompanied by no obvious reduction in search strategies among the rat groups. No impairment of long-term learning and memory in P30 or P60 rats was detected when using a single dose propofol treatment during the most vulnerable period of brain development. DEX was shown to ameliorate the rodent developmental neurotoxicity caused by a single neonatal propofol challenge, by altering MMP-9, BCL2L1 and CC3 apoptotic signaling.

中文翻译：

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右美托咪定对发育中的大脑的神经保护作用是通过减轻单个异丙酚诱导的海马细胞凋亡和突触可塑性缺陷来介导的。

右美托咪定（DEX）具有神经保护作用，其功效已在异丙酚治疗的幼犬中确定。产后一天（P）将7只大鼠暴露于丙泊酚和DEX，以研究诱导的凋亡相关基因表达。此外，通过电子显微镜观察到了细胞水平的突触结构变化。评估了P30大鼠海马长时程增强（LTP）的诱导和在P30和P60时空间分辨的持久表现。在一次异丙酚暴露于P7大鼠后，DEX预处理有效挽救了海马神经细胞中见到的深层细胞凋亡，并强烈逆转了Bcl2-like 1（BCL2L1），基质金属肽酶9（MMP-9）和裂解的caspase 3（ CC3），并大大增强了突触可塑性。然而，探针测试的逃避潜伏时间或穿越时间没有显着差异。这伴随着大鼠组中搜索策略没有明显减少。在最脆弱的大脑发育阶段使用单剂量丙泊酚治疗时，未检测到P30或P60大鼠的长期学习和记忆障碍。事实证明，DEX可以通过改变MMP-9，BCL2L1和CC3的细胞凋亡信号来改善单次新生儿异丙酚攻击引起的啮齿动物发育神经毒性。