Molecules 2012, 17(1), 341-354; doi:10.3390/molecules17010341
Article

Inhibition of Sevoflurane Postconditioning Against Cerebral Ischemia Reperfusion-Induced Oxidative Injury in Rats

1 Department of Anesthesiology, Tianjin Huanhu Hospital, Tianjin 300060, China 2 Department of Pharmacy, Tianjin Huanhu Hospital, Tianjin 300060, China 3 Department of Anesthesiology, The First Hospital Affiliated Shanxi Medical University, Taiyuan, Shanxi 030001, China 4 Metabolic Disease Hospital, Tianjin Medical University, Tianjin 300070, China 5 Key Lab of Hormones and Development, Ministry of Health and Tianjin, Tianjin 300070, China 6 Department of Anesthesiology, Jinghai Hospital, Tianjin 300060, China 7 Department of Anesthesiology, Tangshan City Worker Hospital, Tianjin 300060, China These authors contribute equally to this work.
* Author to whom correspondence should be addressed.
Received: 2 December 2011; in revised form: 23 December 2011 / Accepted: 23 December 2011 / Published: 30 December 2011
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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.
Keywords: antioxidant; immunity; rats; cerebral ischemia reperfusion; TNF-α; sevoflurane postconditioning

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MDPI and ACS Style

Zhang, Y.; Zhang, F.-G.; Meng, C.; Tian, S.-Y.; Wang, Y.-X.; Zhao, W.; Chen, J.; Zhang, X.-S.; Liang, Y.; Zhang, S.-D.; Xing, Y.-J. Inhibition of Sevoflurane Postconditioning Against Cerebral Ischemia Reperfusion-Induced Oxidative Injury in Rats. Molecules 2012, 17, 341-354.

AMA Style

Zhang Y, Zhang F-G, Meng C, Tian S-Y, Wang Y-X, Zhao W, Chen J, Zhang X-S, Liang Y, Zhang S-D, Xing Y-J. Inhibition of Sevoflurane Postconditioning Against Cerebral Ischemia Reperfusion-Induced Oxidative Injury in Rats. Molecules. 2012; 17(1):341-354.

Chicago/Turabian Style

Zhang, Yan; Zhang, Fu-Geng; Meng, Chun; Tian, Shou-Yuan; Wang, Ya-Xin; Zhao, Wei; Chen, Jun; Zhang, Xiu-Shan; Liang, Yu; Zhang, Shi-Dong; Xing, Yan-Jie. 2012. "Inhibition of Sevoflurane Postconditioning Against Cerebral Ischemia Reperfusion-Induced Oxidative Injury in Rats." Molecules 17, no. 1: 341-354.

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