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Postconditioning with sevoflurane protects against focal cerebral ischemia and reperfusion injury via PI3K/Akt pathway.
Brain Res. 2010 Oct 21; 1357:142-51.BR

Abstract

Emerging evidence has demonstrated that postconditioning with sevoflurane provided neuroprotection. In this study, we investigated the neuroprotective effect of different concentrations of sevoflurane in rats with middle cerebral artery occlusion (MCAO). Furthermore, we tested the hypothesis that the neuroprotective effect of postconditioning with sevoflurane is associated with inhibition of apoptosis and mediated by activation of the phosphoinositide-3-kinase/Akt (PI3K/Akt) pathway. Adult male Sprague-Dawley rats were subjected to MCAO for 90 min and then treated with sevoflurane at the beginning of reperfusion. The infarct volume, neurological deficit scores and brain edema were evaluated at 24 hours. Spatial learning and memory was examined by Morris water maze. Apoptosis and apoptosis-related proteins were studied by TUNEL, immunohistochemistry and western blot. The neuroprotective effect and the amount of p-Akt after sevoflurane administration with or without wortmannin were analyzed. Postconditioning with sevoflurane 1.0 minimum alveolar concentration (MAC) and 1.5 MAC significantly decreased neurological deficit scores, infarct volume and brain edema and markedly improved spatial learning and memory. Postconditioning also reduced apoptotic cells, upregulated Bcl-2 and downregulated P53 and Bax. Wortmannin abolished the neuroprotective effect and prevented the increasing of p-Akt. Our data suggest postconditioning with sevoflurane (1.0 MAC and 1.5 MAC) not only reduced infarct volume but also improved learning and memory. Our study further showed that this neuroprotective effect may be partly due to the activation of PI3K/Akt pathway and inhibiting neuronal apoptosis.

Authors+Show Affiliations

Department of Neurosurgery, 2nd Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou 310009, China.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

20705063

Citation

Wang, Jun-Kuan, et al. "Postconditioning With Sevoflurane Protects Against Focal Cerebral Ischemia and Reperfusion Injury Via PI3K/Akt Pathway." Brain Research, vol. 1357, 2010, pp. 142-51.
Wang JK, Yu LN, Zhang FJ, et al. Postconditioning with sevoflurane protects against focal cerebral ischemia and reperfusion injury via PI3K/Akt pathway. Brain Res. 2010;1357:142-51.
Wang, J. K., Yu, L. N., Zhang, F. J., Yang, M. J., Yu, J., Yan, M., & Chen, G. (2010). Postconditioning with sevoflurane protects against focal cerebral ischemia and reperfusion injury via PI3K/Akt pathway. Brain Research, 1357, 142-51. https://doi.org/10.1016/j.brainres.2010.08.009
Wang JK, et al. Postconditioning With Sevoflurane Protects Against Focal Cerebral Ischemia and Reperfusion Injury Via PI3K/Akt Pathway. Brain Res. 2010 Oct 21;1357:142-51. PubMed PMID: 20705063.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Postconditioning with sevoflurane protects against focal cerebral ischemia and reperfusion injury via PI3K/Akt pathway. AU - Wang,Jun-Kuan, AU - Yu,Li-Na, AU - Zhang,Feng-Jiang, AU - Yang,Mei-Juan, AU - Yu,Jing, AU - Yan,Min, AU - Chen,Gao, Y1 - 2010/08/10/ PY - 2010/06/14/received PY - 2010/08/03/revised PY - 2010/08/04/accepted PY - 2010/8/14/entrez PY - 2010/8/14/pubmed PY - 2011/1/15/medline SP - 142 EP - 51 JF - Brain research JO - Brain Res. VL - 1357 N2 - Emerging evidence has demonstrated that postconditioning with sevoflurane provided neuroprotection. In this study, we investigated the neuroprotective effect of different concentrations of sevoflurane in rats with middle cerebral artery occlusion (MCAO). Furthermore, we tested the hypothesis that the neuroprotective effect of postconditioning with sevoflurane is associated with inhibition of apoptosis and mediated by activation of the phosphoinositide-3-kinase/Akt (PI3K/Akt) pathway. Adult male Sprague-Dawley rats were subjected to MCAO for 90 min and then treated with sevoflurane at the beginning of reperfusion. The infarct volume, neurological deficit scores and brain edema were evaluated at 24 hours. Spatial learning and memory was examined by Morris water maze. Apoptosis and apoptosis-related proteins were studied by TUNEL, immunohistochemistry and western blot. The neuroprotective effect and the amount of p-Akt after sevoflurane administration with or without wortmannin were analyzed. Postconditioning with sevoflurane 1.0 minimum alveolar concentration (MAC) and 1.5 MAC significantly decreased neurological deficit scores, infarct volume and brain edema and markedly improved spatial learning and memory. Postconditioning also reduced apoptotic cells, upregulated Bcl-2 and downregulated P53 and Bax. Wortmannin abolished the neuroprotective effect and prevented the increasing of p-Akt. Our data suggest postconditioning with sevoflurane (1.0 MAC and 1.5 MAC) not only reduced infarct volume but also improved learning and memory. Our study further showed that this neuroprotective effect may be partly due to the activation of PI3K/Akt pathway and inhibiting neuronal apoptosis. SN - 1872-6240 UR - https://www.unboundmedicine.com/medline/citation/20705063/Postconditioning_with_sevoflurane_protects_against_focal_cerebral_ischemia_and_reperfusion_injury_via_PI3K/Akt_pathway_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0006-8993(10)01756-7 DB - PRIME DP - Unbound Medicine ER -