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The role of phosphoinositide-3-kinase/Akt pathway in propofol-induced postconditioning against focal cerebral ischemia-reperfusion injury in rats.
Brain Res. 2009 Nov 10; 1297:177-84.BR

Abstract

The aim of this study was to investigate whether propofol could provide postconditioning to ischemic brain injury and the role of phosphoinositide-3-kinase/Akt (PI3K/Akt) pathway in this phenomenon. Rats underwent 2 h of middle cerebral artery occlusion (MCAO) followed by 22 h of reperfusion were randomly divided into nine groups (n=15 each): sham-operated group, MCAO group, propofol 10, 20 and 35 mg x kg(-1) x h(-1) group (propofol 10, 20, 35 mg x kg(-1) x h(-1) infused at the onset of reperfusion for 30 min), wortmannin group (wortmannin 0.6 mg/kg administered 30 min before MCAO), and the other three groups received wortmannin followed by 10, 20 and 35 mg x kg(-1) x h(-1) propofol respectively. Propofol at doses of 10 and 20 mg x kg(-1) x h(-1) significantly reduced infarct volume, decreased neurological deficit scores and attenuated neuron apoptosis compared with MCAO group alone. Increased phosphorylated Akt (P-Akt) was observed in the ischemic penumbra of propofol 10 and 20 mg x kg(-1) x h(-1) group after transient MCAO. The selective PI3K inhibitor, wortmannin partly eliminated the neuroprotective effect and the elevation of P-Akt expression in ischemic penumbra induced by propofol. Propofol at dose of 35 mg x kg(-1) x h(-1) did not affect infarct volume, neurological deficit scores, neuronal apoptosis and the level of P-Akt in transient MCAO rats. Taken together, these results demonstrated that propofol at doses of 10 or 20 mg x kg(-1) x h(-1) infused at the onset of reperfusion for 30 min could provide neuroprotection to transient MCAO rats, and the postconditioning effect induced by propofol partly through maintaining the activity of PI3K/Akt pathway.

Authors+Show Affiliations

Department of Anesthesiology, General Hospital of Tianjin Medical University, Anshan Road No. 154, Heping District, Tianjin, 300052, China.No 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

19703434

Citation

Wang, Hai-yun, et al. "The Role of phosphoinositide-3-kinase/Akt Pathway in Propofol-induced Postconditioning Against Focal Cerebral Ischemia-reperfusion Injury in Rats." Brain Research, vol. 1297, 2009, pp. 177-84.
Wang HY, Wang GL, Yu YH, et al. The role of phosphoinositide-3-kinase/Akt pathway in propofol-induced postconditioning against focal cerebral ischemia-reperfusion injury in rats. Brain Res. 2009;1297:177-84.
Wang, H. Y., Wang, G. L., Yu, Y. H., & Wang, Y. (2009). The role of phosphoinositide-3-kinase/Akt pathway in propofol-induced postconditioning against focal cerebral ischemia-reperfusion injury in rats. Brain Research, 1297, 177-84. https://doi.org/10.1016/j.brainres.2009.08.054
Wang HY, et al. The Role of phosphoinositide-3-kinase/Akt Pathway in Propofol-induced Postconditioning Against Focal Cerebral Ischemia-reperfusion Injury in Rats. Brain Res. 2009 Nov 10;1297:177-84. PubMed PMID: 19703434.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - The role of phosphoinositide-3-kinase/Akt pathway in propofol-induced postconditioning against focal cerebral ischemia-reperfusion injury in rats. AU - Wang,Hai-yun, AU - Wang,Guo-lin, AU - Yu,Yong-hao, AU - Wang,Ying, Y1 - 2009/08/21/ PY - 2009/07/06/received PY - 2009/08/10/revised PY - 2009/08/17/accepted PY - 2009/8/26/entrez PY - 2009/8/26/pubmed PY - 2010/1/9/medline SP - 177 EP - 84 JF - Brain research JO - Brain Res. VL - 1297 N2 - The aim of this study was to investigate whether propofol could provide postconditioning to ischemic brain injury and the role of phosphoinositide-3-kinase/Akt (PI3K/Akt) pathway in this phenomenon. Rats underwent 2 h of middle cerebral artery occlusion (MCAO) followed by 22 h of reperfusion were randomly divided into nine groups (n=15 each): sham-operated group, MCAO group, propofol 10, 20 and 35 mg x kg(-1) x h(-1) group (propofol 10, 20, 35 mg x kg(-1) x h(-1) infused at the onset of reperfusion for 30 min), wortmannin group (wortmannin 0.6 mg/kg administered 30 min before MCAO), and the other three groups received wortmannin followed by 10, 20 and 35 mg x kg(-1) x h(-1) propofol respectively. Propofol at doses of 10 and 20 mg x kg(-1) x h(-1) significantly reduced infarct volume, decreased neurological deficit scores and attenuated neuron apoptosis compared with MCAO group alone. Increased phosphorylated Akt (P-Akt) was observed in the ischemic penumbra of propofol 10 and 20 mg x kg(-1) x h(-1) group after transient MCAO. The selective PI3K inhibitor, wortmannin partly eliminated the neuroprotective effect and the elevation of P-Akt expression in ischemic penumbra induced by propofol. Propofol at dose of 35 mg x kg(-1) x h(-1) did not affect infarct volume, neurological deficit scores, neuronal apoptosis and the level of P-Akt in transient MCAO rats. Taken together, these results demonstrated that propofol at doses of 10 or 20 mg x kg(-1) x h(-1) infused at the onset of reperfusion for 30 min could provide neuroprotection to transient MCAO rats, and the postconditioning effect induced by propofol partly through maintaining the activity of PI3K/Akt pathway. SN - 1872-6240 UR - https://www.unboundmedicine.com/medline/citation/19703434/The_role_of_phosphoinositide_3_kinase/Akt_pathway_in_propofol_induced_postconditioning_against_focal_cerebral_ischemia_reperfusion_injury_in_rats_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0006-8993(09)01773-9 DB - PRIME DP - Unbound Medicine ER -