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Sevoflurane preconditioning attenuates myocardial ischemia/reperfusion injury via caveolin-3-dependent cyclooxygenase-2 inhibition. 2013

Jianli Zhao, and Feng Wang, and Yanqing Zhang, and Liyuan Jiao, and Wayne Bond Lau, and Lili Wang, and Baojiang Liu, and Erhe Gao, and Walter J Koch, and Xin-Liang Ma, and Yajing Wang
Department of Anesthesiology, the First Affiliated Hospital (J.Z., Y.Z., L.J., L.W., B.L.), Department of Pathophysiology (F.W.), and Department of Physiology, Key Laboratory of Cellular Physiology, Ministry of Education (Y.W.), Shanxi Medical University, Taiyuan, China; Department of Emergency Medicine, Thomas Jefferson University, Philadelphia, PA (W.B.L., X.-L.M., Y.W.); and Center for Translational Research, Temple University, Philadelphia, PA (E.G., W.J.K.).

BACKGROUND The inhaled anesthetic sevoflurane has been demonstrated to protect against myocardial ischemia/reperfusion (MI/R) injury via mechanisms involving AMP-activated protein kinase (AMPK) and caveolin-3 (Cav-3). However, the relative contributions of AMPK and Cav-3 to sevoflurane preconditioning (SF-PreCon)-mediated cardioprotection and their precise underlying mechanisms of action remain incompletely understood. RESULTS SF-PreCon (consisting of 3 cycles of 15-minute exposure to 2% sevoflurane before 30 minutes of MI) decreased MI/R injury in wild-type mice (caspase-3 activity, -29.1%; infarct size, -20.2%; and left ventricular end diastolic pressure, -33.8%). In cardiac-specific AMPKα2 dominant-negative overexpressing mice, the cardioprotective effect of SF-PreCon was largely retained (caspase-3 activity, -26.7%; infarct size, -16.7%; and left ventricular end-diastolic pressure, -25.9%; P<0.01). In contrast, SF-PreCon failed to significantly protect Cav-3 knockout mice against MI/R injury (P>0.05). SF-PreCon significantly decreased MI/R-induced superoxide generation in wild-type (-43.6%) and AMPK dominant-negative overexpressing mice (-35.5%; P<0.01) but not in Cav-3 knockout mice. SF-PreCon did not affect nicotinamide adenine dinucleotide phosphate oxidase expression but significantly inhibited cyclooxygenase-2 expression in wild-type (-38.7%) and AMPK dominant-negative overexpressing mice (-35.8%) but not in Cav-3 knockout mice. CONCLUSIONS We demonstrate for the first time SF-PreCon mediates cardioprotection against MI/R injury via caveolin-3-dependent cyclooxygenase-2 inhibition and antioxidative effects.

UI MeSH Term Description Entries
D008297 Male Males
D008738 Methyl Ethers A group of compounds that contain the general formula R-OCH3. Ethers, Methyl
D002478 Cells, Cultured Cells propagated in vitro in special media conducive to their growth. Cultured cells are used to study developmental, morphologic, metabolic, physiologic, and genetic processes, among others. Cultured Cells,Cell, Cultured,Cultured Cell
D000077149 Sevoflurane A non-explosive inhalation anesthetic used in the induction and maintenance of general anesthesia. It does not cause respiratory irritation and may also prevent PLATELET AGGREGATION. BAX 3084,Fluoromethyl Hexafluoroisopropyl Ether,Fluoromethyl-2,2,2-trifluoro-1-(trifluoromethyl)ethyl Ether,Sevorane,Ultane
D000818 Animals Unicellular or multicellular, heterotrophic organisms, that have sensation and the power of voluntary movement. Under the older five kingdom paradigm, Animalia was one of the kingdoms. Under the modern three domain model, Animalia represents one of the many groups in the domain EUKARYOTA. Animal,Metazoa,Animalia
D015428 Myocardial Reperfusion Injury Damage to the MYOCARDIUM resulting from MYOCARDIAL REPERFUSION (restoration of blood flow to ischemic areas of the HEART.) Reperfusion takes place when there is spontaneous thrombolysis, THROMBOLYTIC THERAPY, collateral flow from other coronary vascular beds, or reversal of vasospasm. Reperfusion Injury, Myocardial,Injury, Myocardial Reperfusion,Myocardial Ischemic Reperfusion Injury,Injuries, Myocardial Reperfusion,Myocardial Reperfusion Injuries,Reperfusion Injuries, Myocardial
D051244 Caveolin 3 A caveolin that is expressed exclusively in MUSCLE CELLS and is sufficient to form CAVEOLAE in SARCOLEMMA. Mutations in caveolin 3 are associated with multiple muscle diseases including DISTAL MYOPATHY and LIMB-GIRDLE MUSCULAR DYSTROPHY. Caveolin-3,M-Caveolin,Muscle Caveolin,Caveolin, Muscle
D051379 Mice The common name for the genus Mus. Mice, House,Mus,Mus musculus,Mice, Laboratory,Mouse,Mouse, House,Mouse, Laboratory,Mouse, Swiss,Mus domesticus,Mus musculus domesticus,Swiss Mice,House Mice,House Mouse,Laboratory Mice,Laboratory Mouse,Mice, Swiss,Swiss Mouse,domesticus, Mus musculus
D052246 Cyclooxygenase 2 Inhibitors A subclass of cyclooxygenase inhibitors with specificity for CYCLOOXYGENASE-2. COX-2 Inhibitor,COX2 Inhibitor,Coxib,Cyclooxygenase 2 Inhibitor,Cyclooxygenase-2 Inhibitor,COX-2 Inhibitors,COX2 Inhibitors,Coxibs,Cyclooxygenase-2 Inhibitors,2 Inhibitor, Cyclooxygenase,COX 2 Inhibitor,COX 2 Inhibitors,Inhibitor, COX-2,Inhibitor, COX2,Inhibitor, Cyclooxygenase 2,Inhibitor, Cyclooxygenase-2,Inhibitors, COX-2,Inhibitors, COX2,Inhibitors, Cyclooxygenase 2,Inhibitors, Cyclooxygenase-2
D018345 Mice, Knockout Strains of mice in which certain GENES of their GENOMES have been disrupted, or "knocked-out". To produce knockouts, using RECOMBINANT DNA technology, the normal DNA sequence of the gene being studied is altered to prevent synthesis of a normal gene product. Cloned cells in which this DNA alteration is successful are then injected into mouse EMBRYOS to produce chimeric mice. The chimeric mice are then bred to yield a strain in which all the cells of the mouse contain the disrupted gene. Knockout mice are used as EXPERIMENTAL ANIMAL MODELS for diseases (DISEASE MODELS, ANIMAL) and to clarify the functions of the genes. Knockout Mice,Mice, Knock-out,Mouse, Knockout,Knock-out Mice,Knockout Mouse,Mice, Knock out

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