N-acetylcysteine (NAC) is known to serve many biological functions including acting as an antioxidant, and electing antiinflammatory effects. Previous reports have revealed that NAC may have neuroprotective effects against the deleterious effects of brain ischemia. Despite of this, the mechanism by which NAC prevents neuronal damage after brain ischemia remains unclear. The current study aimed to investigate this mechanism in a mouse model of transient global brain ischemia. In the present study, mice were subjected to 20 min of transient global brain ischemia, proceeded by intraperitoneal administration of NAC (150 mg/kg) in one group. The mice were then euthanized 72 h after this ischemic insult for collection of experimental tissues. The effect of NAC on neuronal damage and matrix metalloproteinase (MMP)-9 activity were assessed and immunofluorescence, and hippocampal terminal deoxynucleotidyl transferase-mediated dUTP nick end-labeling (TUNEL) assay experiments were conducted and results compared between NAC- and vehicle-treated groups. Neuronal damage was primarily observed in the hippocampal CA1 and CA2 regions. In NAC-treated mice, neuronal damage was significantly reduced after ischemia when compared to vehicle-treated animals. NAC also inhibited increased MMP-9 activity after global brain ischemia. NAC increased laminin and NeuN expression and inhibited increases in TUNEL-positive cells, all in the hippocampus. These results suggest that NAC reduces hippocampal neuronal damage following transient global ischemia, potentially via reductions in MMP-9 activity.

中文翻译：

---

N-乙酰半胱氨酸在短暂性全脑缺血小鼠模型中通过抑制基质金属蛋白酶的神经保护作用。

已知N-乙酰半胱氨酸（NAC）具有许多生物学功能，包括充当抗氧化剂和发挥抗炎作用。先前的报道显示NAC可能对脑缺血的有害作用具有神经保护作用。尽管如此，NAC预防脑缺血后神经元损伤的机制仍不清楚。当前的研究旨在研究短暂性全脑缺血的小鼠模型中的这种机制。在本研究中，对小鼠进行20分钟的短暂性全脑缺血，然后在一组中通过腹膜内给予NAC（150 mg / kg）进行治疗。然后在缺血性损伤后72小时对小鼠实施安乐死以收集实验组织。评估了NAC对神经元损伤和基质金属蛋白酶（MMP）-9活性的影响并进行了免疫荧光分析，并进行了海马末端脱氧核苷酸转移酶介导的dUTP缺口末端标记（TUNEL）分析实验，并比较了NAC和媒介物处理后的结果组。神经元损伤主要在海马CA1和CA2区观察到。在NAC处理的小鼠中，与媒介物处理的动物相比，缺血后神经元的损伤明显减少。在全脑缺血后，NAC还抑制了MMP-9活性的增加。NAC增加海马中层粘连蛋白和NeuN的表达，并抑制TUNEL阳性细胞的增加。这些结果表明，NAC可能通过降低MMP-9活性来减轻短暂性全局缺血后海马神经元的损害。并进行了海马末端脱氧核苷酸转移酶介导的dUTP缺口末端标记（TUNEL）分析实验，并比较了NAC组和媒介物处理组之间的结果。神经元损伤主要在海马CA1和CA2区观察到。在NAC处理的小鼠中，与媒介物处理的动物相比，缺血后神经元的损伤明显减少。在全脑缺血后，NAC还抑制了MMP-9活性的增加。NAC增加海马中层粘连蛋白和NeuN的表达，并抑制TUNEL阳性细胞的增加。这些结果表明，NAC可能通过降低MMP-9活性来减轻短暂性全局缺血后海马神经元的损害。并进行了海马末端脱氧核苷酸转移酶介导的dUTP缺口末端标记（TUNEL）分析实验，并比较了NAC组和媒介物处理组之间的结果。神经元损伤主要在海马CA1和CA2区观察到。在NAC处理的小鼠中，与媒介物处理的动物相比，缺血后神经元的损伤明显减少。在全脑缺血后，NAC还抑制了MMP-9活性的增加。NAC增加海马中层粘连蛋白和NeuN的表达，并抑制TUNEL阳性细胞的增加。这些结果表明，NAC可能通过降低MMP-9活性来减轻短暂性全局缺血后海马神经元的损害。