Busse Johanna Franziska, Frai Jonas, Hamacher Luca Ines, Matschke Veronika, Theiss Carsten, Weber Thomas, Herzog-Niescery Jennifer, Stahlke Sarah
Institute of Anatomy, Department of Cytology, Ruhr-University Bochum, 44801 Bochum, Germany.
International Graduate School of Neuroscience (IGSN), Ruhr-University Bochum, 44801 Bochum, Germany.
Int J Mol Sci. 2025 Sep 16;26(18):9019. doi: 10.3390/ijms26189019.
Global cerebral hypoxia triggers (mal-)adaptive responses that can lead to neuronal damage. This study evaluated edaravone's neuroprotective effects in a rat hypoxia model, focusing on sex differences, treatment durations, and behavioral outcomes. Male and female rats underwent global cerebral hypoxia induced by rocuronium, with post-hypoxia edaravone treatment. Motor coordination and activity were assessed through exploratory behavior tests. Histological analyses evaluated neuronal integrity and apoptosis, while microglial activity and gene expression were analyzed via immunofluorescence and qPCR. Edaravone showed transient neuroprotective effects on motor behavior and early immune responses, particularly in the cerebellum and hippocampus. No gross morphological damage was observed, though functional impairments occurred despite preserved cytoarchitecture. Microglial activity was initially suppressed in treated and later activated in untreated hypoxic brains, suggesting modulating immune responses. Gene expression analysis revealed region-specific, time-dependent, and sex-specific changes, including early upregulation of CCR7, S100B, and NSE in treated animals. Males were more susceptible to hypoxic damage, while females showed higher baseline resistance and better functional recovery. Seven-day edaravone treatment increased apoptotic markers in male cerebellum, indicating sex-specific differences in cell death mechanisms. These findings highlight the potential for personalized therapy and underscore the importance of considering sex differences in both research and clinical practice.
全脑缺氧会引发(不良)适应性反应,进而导致神经元损伤。本研究评估了依达拉奉在大鼠缺氧模型中的神经保护作用,重点关注性别差异、治疗持续时间和行为结果。雄性和雌性大鼠接受罗库溴铵诱导的全脑缺氧,并在缺氧后给予依达拉奉治疗。通过探索行为测试评估运动协调性和活动情况。组织学分析评估神经元完整性和凋亡,同时通过免疫荧光和定量聚合酶链反应分析小胶质细胞活性和基因表达。依达拉奉对运动行为和早期免疫反应显示出短暂的神经保护作用,尤其是在小脑和海马体中。尽管细胞结构得以保留,但仍出现了功能障碍,未观察到明显的形态学损伤。在接受治疗的缺氧大脑中,小胶质细胞活性最初受到抑制,随后在未接受治疗的缺氧大脑中被激活,这表明其对免疫反应具有调节作用。基因表达分析揭示了区域特异性、时间依赖性和性别特异性变化,包括治疗动物中趋化因子受体7、S100B和神经元特异性烯醇化酶的早期上调。雄性对缺氧损伤更敏感,而雌性表现出更高的基线抵抗力和更好的功能恢复。为期七天的依达拉奉治疗增加了雄性小脑的凋亡标志物,表明细胞死亡机制存在性别特异性差异。这些发现凸显了个性化治疗的潜力,并强调了在研究和临床实践中考虑性别差异的重要性。