@article {2650,
	title = {Propofol protects against hydrogen peroxide-induced injury in cardiac H9c2 cells via Akt activation and Bcl-2 up-regulation},
	journal = {Biochemical and Biophysical Research Communications},
	volume = {389},
	number = {1},
	year = {2009},
	note = {ISI Document Delivery No.: 555SMTimes Cited: 4Cited Reference Count: 26Wang, Baohua Shravah, Jayant Luo, Honglin Raedschelders, Koen Chen, David D. Y. Ansley, David M.},
	month = {Nov},
	pages = {105-111},
	type = {Article},
	abstract = {<p>Propofol is a widely used intravenous anesthetic agent with antioxidant properties secondary to its phenol based chemical structure. Treatment with propofol has been found to attenuate oxidative stress and prevent ischemia/reperfusion injury in rat heart. Here, we report that propofol protects cardiac H9c2 cells from hydrogen peroxide (H2O2)-induced injury by triggering the activation of Akt and a parallel up-regulation of Bcl-2. We show that pretreatment with propofol significantly protects against H2O2-induced injury. We further demonstrate that propofol activates the PI3K-Akt signaling pathway. The protective effect of propofol on H2O2-induced injury is reversed by PI3K inhibitor wortmannin, which effectively suppresses propofol-induced activation of Akt, up-regulation of Bcl-2, and protection from apoptosis. Collectively, our results reveal a new mechanism by which propofol inhibits H2O2-induced injury in cardiac H9c2 cells, supporting a potential application of propofol as a preemptive cardioprotectant in clinical settings such as coronary bypass surgery. (C) 2009 Elsevier Inc. All rights reserved.</p>},
	keywords = {15-F-2T-ISOPROSTANE FORMATION, Akt, antioxidant capacity, apoptosis, Bcl-2, CARDIOMYOCYTES, ENDOTHELIAL-CELLS, H9c2 cells, INJURY, KINASE-C, OXIDATIVE STRESS, Propofol, RAT-HEART, REDUCES APOPTOSIS, REPERFUSION, SENSITIVITY, SURVIVAL},
	isbn = {0006-291X},
	doi = {doi: 10.1016/j.bbrc.2009.08.097},
	url = {<Go to ISI>://000274534900020},
	author = {Wang, B. H. and Shravah, J. and Luo, H. L. and Raedschelders, K. and Chen, D. D. Y. and Ansley, D. M.}
}
