Neuroprotective effects of sevoflurane against electromagnetic pulse-induced brain injury through inhibition of neuronal oxidative stress and apoptosis

• Published in: PloS one 2014-03, Vol.9 (3), p.e91019
• Main Authors: Deng, Bin, Xu, Hao, Zhang, Jin, Wang, Jin, Han, Li-Chun, Li, Li-Ya, Wu, Guang-Li, Hou, Yan-Ning, Guo, Guo-Zhen, Wang, Qiang, Sang, Han-Fei, Xu, Li-Xian
• Format: Article
• Language: English
• Subjects: Anesthetic gases; Animals; Apoptosis; Apoptosis - drug effects; bcl-2-Associated X Protein - metabolism; Behavior, Animal - drug effects; Biology; Brain damage; Brain injuries; Brain Injuries - complications; Brain Injuries - drug therapy; Brain Injuries - pathology; Caspase 3 - metabolism; Cell Survival - drug effects; Central nervous system; Cerebral Cortex - pathology; Cognition - drug effects; Electromagnetic Fields; Electromagnetism; Electron microscopy; L-Lactate Dehydrogenase - metabolism; Learning; Male; Malondialdehyde - metabolism; Medicine; Memory; Methyl Ethers - pharmacology; Methyl Ethers - therapeutic use; Nerve Degeneration - complications; Nerve Degeneration - drug therapy; Nerve Degeneration - pathology; Neurons; Neurons - drug effects; Neurons - enzymology; Neurons - pathology; Neurons - ultrastructure; Neuroprotective Agents - pharmacology; Occupational safety and health; Oxidative stress; Oxidative Stress - drug effects; Radiation; Rats, Sprague-Dawley; Sevoflurane; Superoxide dismutase; Superoxide Dismutase - metabolism; Superoxides
• ISSN: 1932-6203; 1932-6203
• DOI: 10.1371/journal.pone.0091019

Electromagnetic pulse (EMP) causes central nervous system damage and neurobehavioral disorders, and sevoflurane protects the brain from ischemic injury. We investigated the effects of sevoflurane on EMP-induced brain injury. Rats were exposed to EMP and immediately treated with sevoflurane. The protective effects of sevoflurane were assessed by Nissl staining, Fluoro-Jade C staining and electron microscopy. The neurobehavioral effects were assessed using the open-field test and the Morris water maze. Finally, primary cerebral cortical neurons were exposed to EMP and incubated with different concentration of sevoflurane. The cellular viability, lactate dehydrogenase (LDH) release, superoxide dismutase (SOD) activity and malondialdehyde (MDA) level were assayed. TUNEL staining was performed, and the expression of apoptotic markers was determined. The cerebral cortexes of EMP-exposed rats presented neuronal abnormalities. Sevoflurane alleviated these effects, as well as the learning and memory deficits caused by EMP exposure. In vitro, cell viability was reduced and LDH release was increased after EMP exposure; treatment with sevoflurane ameliorated these effects. Additionally, sevoflurane increased SOD activity, decreased MDA levels and alleviated neuronal apoptosis by regulating the expression of cleaved caspase-3, Bax and Bcl-2. These findings demonstrate that Sevoflurane conferred neuroprotective effects against EMP radiation-induced brain damage by inhibiting neuronal oxidative stress and apoptosis.