Sevoflurane and Isoflurane Preconditioning Provides Neuroprotection by Inhibition of Apoptosis-related mRNA Expression in a Rat Model of Focal Cerebral Ischemia

作者：Nurdan Bedirli, Emin Ümit Bağrıaçık, Hakan Emmez, Güldal Yılmaz, Yusuf Ünal, Zerrin Özköse · 发表于：Journal of Neurosurgical Anesthesiology · 年份：2012 · DOI：10.1097/ana.0b013e318266791e · 被引用次数：79 · 研究领域：Cardiac Ischemia and Reperfusion、Anesthesia and Neurotoxicity Research、Neuroinflammation and Neurodegeneration Mechanisms

BACKGROUND: This study aimed to examine the effects of sevoflurane or isoflurane preconditioning on cerebral ischemia/reperfusion-induced inflammation, oxidative stress, and lipid peroxidation and test the hypothesis that the underlining mechanism of the protective effect of preconditioning involves changes in the apoptotic gene expression profiles in an experimental model of middle cerebral artery occlusion in rats. METHODS: Twenty-four adult male rats were randomly divided into 3 groups: control (n=8), sevoflurane (n=8), and isoflurane (n=8). For preconditioning, these 3 groups were exposed to 40% O2, 2% sevoflurane, and 1.5% isoflurane, respectively, for 60 minutes, followed immediately by 1 hour of middle cerebral artery occlusion and then 6 hours of reperfusion. Blood and brain tissue samples were collected for determination of blood gas tension, tumor necrosis factor-α, interleukin-6, and interleukin-1β. Brain tissue samples were collected for determination of the wet/dry ratio, myeloperoxidase, malondialdehyde, and total RNA and also for histologic examinations. RESULTS: Tumor necrosis factor-α, interleukin-1β, and myeloperoxidase levels decreased and antioxidant enzyme levels increased in the sevoflurane group compared with the control and isoflurane groups. Proapoptotic genes (Tnf, Tnfrsf10b, and Tp53) downregulated and antiapoptotic genes (Aven, Bcl2, Bcl2l2, and Prok2) upregulated with sevoflurane treatment compared with the isoflurane and control groups. Both isof...