Journal
BEHAVIOURAL BRAIN RESEARCH
Volume 405, Issue -, Pages -Publisher
ELSEVIER
DOI: 10.1016/j.bbr.2021.113200
Keywords
Nuclear factor erythroid-2-related factor-2; Heme oxygenase-1; Sevoflurane; Cognition; Traumatic brain injury
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Funding
- Project of Health Committee of Tianjin Province of China [2019044]
- National Natural Science Foundation of China [81772106]
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Sevoflurane administered immediately after TBI can protect against TBI-induced synaptic and cognitive impairments by promoting the antioxidant Nrf-2/HO-1 pathway, making it a promising anesthetic for patients with TBI.
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.
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