292 research outputs found
Discovery and characterization of novel, potent, and selective cytochrome P450 2J2 inhibitors.
Dialkyl and Methyl-Alkyl Zirconocenes: Synthesis and Characterization of Zirconocene-Alkyls That Model the Polymeryl Chain in Alkene Polymerizations
Progress toward Device-Quality Second-Order Nonlinear Optical Materials. 4. A Trilink High μβ NLO Chromophore in Thermoset Polyurethane: A “Guest−Host” Approach to Larger Electrooptic Coefficients
Triacsin C, a fatty acyl coA synthetase inhibitor, improves cardiac performance following global ischemia.
Abstract The role of fatty acyl CoA synthetase (FACS) in ischemia/reperfusion (I/R) injury has not been well established. Our earlier studies showed that triacsin C, a selective FACS inhibitor, decreases endothelial nitric oxide synthase (eNOS) palmitoylation and increases nitric oxide (NO) in cultured human coronary endothelial cells. In the present study, we tested the hypothesis that triacsin C would reduce infarct size and improve post-reperfusion cardiac function by increasing vascular NO. In isolated rat hearts, triacsin C, given during the first 5 minutes of reperfusion, significantly reduced infarct size and attenuated cardiac dysfunction during reperfusion. N G -nitro-L-arginine methyl ester (L-NAME, a non-selective NOS inhibitor, 50 µM) completely abolished the protective effects of triacsin C. In the ischemic hind limb model, triacsin C significantly increased intravascular NO concentration during reperfusion, an effect that was blocked by L-NAME or S-methyl-L-thiocitrulline (SMTC, a selective neuronal NOS inhibitor), but not by 1400W (a highly selective iNOS inhibitor). Lastly, triacsin C significantly reduced L-NAME induced leukocyte rolling, adhesion, and transmigration in rat mesenteric circulation, as measured by intravital microscopy. In summary, this study provides novel evidence showing that triacsin C reduces myocardial infarct size, attenuates loss of post-reperfusion cardiac function, increases intravascular NO concentration and inhibits leukocyte recruitment. These pharmacologic properties suggest that triacsin C may be useful as an adjunct to Am
Synthesis of Block Copolymers Containing Pendant Carbazole Groups via Living Ring-Opening Metathesis Polymerization
Thiazolidinediones mimic glucose starvation in facilitating Sp1 degradation through the up-regulation of beta-transducin repeat-containing protein. Mol Pharmacol 76
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