Departamento de Química, Centro de Ciências Naturais e Exatas, Universidade Federal de Santa Maria, Campus Universitário, Camobi, Santa Maria, RS, Brazil.
Mol Cell Biochem. 2013 Jun;378(1-2):247-55. doi: 10.1007/s11010-013-1615-9. Epub 2013 Mar 21.
Perinatal hypoxic-ischemic (HI) brain injury is a common problem with severe neurologic sequelae. The definitive brain injury is a consequence of pathophysiological mechanisms that begin at the moment of HI insult and may extend for days or weeks. In this context, the inflammatory response and the formation of reactive oxygen species seem to play a key role during evolution of brain damage after injury. Thus, the aim of this study was to describe the chronological sequence of acetylcholinesterase (AChE) activity and the lipid peroxidation changes in the cerebral cortex using the classic model of neonatal HI. Furthermore, the erythrocyte AChE and adenosine deaminase (ADA) activities as well as the serum levels of proinflammatory cytokines were assessed. We observed that neonatal HI caused an increase of lipid peroxidation immediately after HI insult, which remained for several days afterward. There was a time-related change in the AChE activity in the cerebral cortex and the same was observed in erythrocyte AChE and ADA activities. In addition, immediately after HI, ADA activity showed a strong positive correlation with all proinflammatory cytokines assessed. Together, these findings may help the understanding of some mechanism related to the pathophysiology of neonatal HI, therefore highlighting the putative therapeutic targets to minimize brain injury and enhance recovery.
围产期缺氧缺血性（HI）脑损伤是一种常见的严重神经后遗症问题。明确的脑损伤是病理生理机制的结果，这些机制从 HI 损伤的那一刻开始，并可能持续数天或数周。在这种情况下，炎症反应和活性氧的形成似乎在损伤后脑损伤的演变过程中发挥关键作用。因此，本研究旨在描述使用经典新生 HI 模型，大脑皮层乙酰胆碱酯酶（AChE）活性和脂质过氧化变化的时间顺序。此外，还评估了红细胞 AChE 和腺苷脱氨酶（ADA）活性以及促炎细胞因子的血清水平。我们观察到，新生 HI 导致 HI 损伤后立即增加脂质过氧化，此后持续数天。大脑皮层中的 AChE 活性以及红细胞 AChE 和 ADA 活性均发生了与时间相关的变化。此外，HI 后立即，ADA 活性与所有评估的促炎细胞因子呈强烈正相关。综上所述，这些发现可能有助于理解与新生 HI 病理生理学相关的一些机制，从而突出潜在的治疗靶点，以最大程度地减少脑损伤并促进恢复。
