@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.}
}
@article {2350,
	title = {Rationale, design and baseline characteristics of the PROJECT II study: PROpofol CardioproTECTion for Type II diabetics A randomized, controlled trial of high-dose propofol versus isoflurane preconditioning in patients undergoing on-pump coronary artery b},
	journal = {Contemporary Clinical Trials},
	volume = {30},
	number = {4},
	year = {2009},
	note = {ISI Document Delivery No.: 456NPTimes Cited: 1Cited Reference Count: 23Ansley, David M. Raedschelders, Koen Chen, David D. Y. Choi, Peter T.},
	month = {Jul},
	pages = {380-385},
	type = {Article},
	abstract = {Diabetes mellitus is a leading cause of death globally and results in significant morbidity and mortality following surgery. After cardiac surgery, diabetic patients are especially at risk for low cardiac output syndrome, which can quadruple the risk for postoperative death. Attempts to prevent low cardiac output syndrome have focused on increasing myocardial tolerance to ischemia (preconditioning), which involves the myocardial mitochondrial ATP-regulated K-ATP channel. G-protein initiation, nitric oxide synthase, and protein kinase C. Unfortunately, the signal transduction pathways required for preconditioning are corrupted in diabetes. Effective antioxidant intervention during ischemia-reperfusion appears important for preserving myocardial function: thus, alleviating oxidant-mediated post-ischemic injury by increasing antioxidant defenses (cardioprotection) is an alternative to preconditioning. Our previous work suggests that propofol(2,6-diisopropylphenol), an intravenous anesthetic with antioxidant potential, may confer cardioprotection. In this paper, we describe the rationale and methodology of the Pro-TECT II Study, a Phase II randomized controlled trial designed to explore the relationships of biomarkers of oxidative or nitrosative stress in diabetes, to determine the effect of propofol cardioprotection to counteract these effects in patients undergoing elective primary coronary bypass graft surgery with cardiopulmonary bypass, and to provide feasibility and sample size data needed to conduct Phase III trials. (C) 2009 Elsevier Inc. All rights reserved.},
	keywords = {15-F-2T-ISOPROSTANE FORMATION, antioxidant, apoptosis, CAPACITY, Cardiopulmonary bypass, Diabetes mellitus, EXPRESSION, F2-isoprostanes, HYPERGLYCEMIA, INJURY, MORTALITY, MYOCARDIAL-INFARCTION, Nitric oxide synthase type III, PREDICTORS, Propofol, SHORT-TERM},
	isbn = {1551-7144},
	url = {<Go to ISI>://000266853900014},
	author = {Ansley, D. M. and Raedschelders, K. and Chen, D. D. Y. and Choi, P. T.}
}
