Department of Anesthesiology and Critical Care Medicine, Tianjin NanKai Hospital, Tianjin Medical University, Tianjin, 300100, China.
Tianjin Medical University, Tianjin, 300070, China.
Behav Brain Res. 2021 May 7;405:113200. doi: 10.1016/j.bbr.2021.113200. Epub 2021 Feb 23.
Traumatic brain injury (TBI) is an increasingly common emergency disease that usually leads to prolonged physical and cognitive impairments. In this study, we investigated if sevoflurane could induce cognitive improvement in TBI rats. Rats were subjected to head trauma induced by a fluid percussion device. A two-hour exposure to 3% sevoflurane was performed in a chamber immediately after TBI. Sevoflurane inhalation reduced the neurological and cognitive deficits induced by TBI with ameliorated synaptic injuries in the hippocampus. Moreover, after sevoflurane treatment, the expression of nuclear factor erythroid-2-related factor-2 (Nrf-2) and hemeoxygenase-1 (HO-1) in the hippocampus was enhanced 1 d after TBI and maintained at high levels 14 days later, and oxidative stress induced by TBI was inhibited. However, the HO-1 inhibitor, Zinc protoporphyrin (ZnPP), used to demonstrate the involvement of HO-1, suppressed the protective effect of sevoflurane. These results indicate that sevoflurane administered immediately after TBI may protect against TBI-induced synaptic and cognitive impairments by promoting the antioxidant Nrf-2/HO-1 pathway. Sevoflurane may be a promising anesthetic for patients with TBI.
颅脑损伤（TBI）是一种日益常见的急诊疾病，通常会导致长期的身体和认知障碍。在这项研究中，我们研究了七氟醚是否能诱导 TBI 大鼠的认知改善。大鼠通过液体冲击装置受到颅脑创伤。在 TBI 后立即在室中暴露于 3%七氟醚 2 小时。七氟醚吸入可减轻 TBI 引起的神经和认知缺陷，并改善海马中的突触损伤。此外，七氟醚治疗后，TBI 后 1 天海马核因子红细胞 2 相关因子 2（Nrf-2）和血红素加氧酶-1（HO-1）的表达增强，并维持在高水平 14 天后，TBI 引起的氧化应激受到抑制。然而，HO-1 抑制剂锌原卟啉（ZnPP）用于表明 HO-1 的参与，抑制了七氟醚的保护作用。这些结果表明，TBI 后立即给予七氟醚可能通过促进抗氧化 Nrf-2/HO-1 途径来保护 TBI 引起的突触和认知障碍。七氟醚可能是 TBI 患者有前途的麻醉剂。
