During chronic inflammatory disease, such asthma, leukocytes can invade the central nervous system (CNS) and together with CNS-resident cells, generate excessive reactive oxygen species (ROS) production as well as disbalance in the antioxidant system, causing oxidative stress, which contributes a large part to neuroinflammation. In this sense, the aim of this study is to investigate the effects of treatment with neostigmine, known for the ability to control lung inflammation, on oxidative stress in the cerebral cortex of asthmatic mice. Female BALB/cJ mice were submitted to asthma model induced by ovalbumin (OVA). Control group received only Dulbecco's phosphate-buffered saline (DPBS). To evaluate neostigmine effects, mice received 80 μg/kg of neostigmine intraperitoneally 30 min after each OVA challenge. Our results revealed for the first time that treatment with neostigmine (an acetylcholinesterase inhibitor that no crosses the BBB) was able to revert ROS production and change anti-oxidant enzyme catalase in the cerebral cortex in asthmatic mice. These results support the communication between the peripheral immune system and the CNS and suggest that acetylcholinesterase inhibitors, such as neostigmine, should be further studied as possible therapeutic strategies for neuroprotection in asthma.

中文翻译：

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新斯的明治疗诱导哮喘小鼠大脑皮层氧化应激的神经保护作用。

在慢性炎症性疾病（如哮喘）期间，白细胞可侵入中枢神经系统 (CNS) 并与中枢神经系统驻留细胞一起产生过多的活性氧 (ROS) 以及抗氧化系统失衡，导致氧化应激，这有助于很大一部分是神经炎症。从这个意义上说，本研究的目的是研究新斯的明（以控制肺部炎症的能力而闻名）治疗对哮喘小鼠大脑皮层氧化应激的影响。将雌性 BALB/cJ 小鼠置于由卵清蛋白 (OVA) 诱导的哮喘模型中。对照组仅接受 Dulbecco 磷酸盐缓冲盐水 (DPBS)。为了评估新斯的明作用，小鼠在每次 OVA 攻击后 30 分钟腹膜内接受 80 μg/kg 的新斯的明。我们的研究结果首次表明，用新斯的明（一种不穿过 BBB 的乙酰胆碱酯酶抑制剂）治疗能够逆转哮喘小鼠大脑皮层中的 ROS 产生并改变抗氧化酶过氧化氢酶。这些结果支持外周免疫系统和 CNS 之间的交流，并表明应该进一步研究乙酰胆碱酯酶抑制剂，如新斯的明，作为哮喘神经保护的可能治疗策略。