Abstract
The volatile anesthetic sevoflurane is capable of inducing preconditioning and postconditioning effects in the brain. In this study, we investigated the effects of sevoflurane postconditioning on antioxidant and immunity indexes in cerebral ischemia reperfusion (CIR) rats. Rats were randomly assigned to five separate experimental groups I–V. In the sham group (I), rats were subjected to the same surgery procedures except for occlusion of the middle cerebral artery and exposed to 1.0 MAC sevoflurane 90 min after surgery for 30 min. IR control rats (group II) were subjected to middle cerebral artery occlusion (MCAO) for 90 min and exposed to O2 for 30 min at the beginning of reperfusion. Sevoflurane 0.5, 1.0 and 1.5 groups (III, IV, V) were all subjected to MCAO for 90 min, but at the beginning of reperfusion exposed to 0.5 MAC, 1.0 MAC or 1.5 MAC sevoflurane for 30 min, respectively. Results showed that sevoflurane postconditioning can decrease serum tumor necrosis factor-alpha (TNF-α), interleukin-1 beta (IL-1β), nitric oxide (NO), nitric oxide synthase (NOS) and increase serum interleukin-10 (IL-10) levels in cerebral ischemia reperfusion rats. In addition, sevoflurane postconditioning can still decrease blood lipid, malondialdehyde (MDA) levels, infarct volume and increase antioxidant enzymes activities, normal pyramidal neurons density in cerebral ischemia reperfusion rats. It can be concluded that sevoflurane postconditioning may decrease blood and brain oxidative injury and enhance immunity indexes in cerebral ischemia reperfusion rats.
Highlights
Oxidation, which provides energy to biological processes, is essential to organisms
We examine the protective effect of sevoflurane postconditioning against oxidative injury in cerebral ischemia reperfusion rats
The present study shows that elevation of MDA and depletion of protective enzymes (SOD, CAT, and GSH-Px) in ischemic reperfused brain are in agreement with earlier reports [50]
Summary
Oxidation, which provides energy to biological processes, is essential to organisms. reactive oxygen species, which are continuously generated when oxygen is reduced by single electrons in vivo, can cause extensive damage to lipids, proteins, DNA and other components of organisms. Cerebral ischemia is one of the leading causes for several neurological deficits and death [8] and the causative mechanism suggested explaining this phenomenon is the involvement of reactive oxygen species (ROS) and oxidative stress [9,10]. Extensive research has been done to find effective strategies and drugs to ameliorate or prevent brain ischemia and reperfusion injury Many anesthetics such as propofol [13,14] and dexmedetomidine [15,16] have neuroprotective effects. Yu et al [19] examined the role of the phosphatidylinositol-3-kinase (PI3K)/Akt pathway in anesthetic postconditioning and determined whether PI3K/Akt signaling modulates the expression of pro- and antiapoptotic proteins in sevoflurane postconditioning. We examine the protective effect of sevoflurane postconditioning against oxidative injury in cerebral ischemia reperfusion rats
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