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Ischemia-reperfusion injury models

Apart from these two Vertex compounds, only one other caspase inhibitor, BDN-6556, has been used in clinical trials. This compound belongs to the class of oxamyl dipeptides and was originally developed by Idun Pharmaceuticals (taken over by Pfizer). It is the only pan-caspase inhibitor that has been evaluated in humans. BDN-6556 displays inhibitory activity against all tested human caspases. It is also an irreversible, caspase-specific inhibitor that does not inhibit other major classes of proteases, or other enzymes or receptors. The therapeutic potential of BDN-6556 was first evaluated in several animal models of liver disease because numerous publications suggested that apoptosis contributes substantially to the development of some hepatic diseases, such as alcoholic hepatitis, hepatitis B and C (HBV, HCV), non-alcoholic steato-hepatitis (NASH), and ischemia/reperfusion injury associated with liver transplant. Accordingly, BDN-6556 was tested in a phase I study. The drug was safe and... [Pg.333]

Ischemia-reperfusion is thought to mediate the severe organ dysfunction witnessed after shock or cardiac arrest. HSPs could play a major role in the defence against ischemia-reperfusion injury. Many in vivo experimental models of ischemia and/or ischemia-reperfusion have demonstrated HSP induction. [Pg.68]

Recently, monoclonal antibodies were attached to gas-filled microbubbles using this spacer coupHng technology. Testing in vitro, in a cell culture system, demonstrated selective accumulation of decafluorobutane-based lipid shell MP1950 microbubbles with covalently attached anti-lCAM-1 antibodies, onto the surface of activated endotheUum [8]. Anti-P-selectin antibodies attached to such microbubbles via an avidin-biotin scheme showed selective accumulation in the areas of inflammation and ischemia/reperfusion injury in an animal model [93]. In the latter example, biotin was also connected to the microbubble surface via a flexible polymer spacer arm. [Pg.101]

Given the intense interest on adenosine and adenosine receptor-induced cytoprotec-tive effects, a number of biological models have been developed to study the role of each receptor subtype and to investigate its underlying signaling mechanism. Historically, research on the protective action of adenosine A3 receptors began with protection of the heart from ischemia/reperfusion injury. A growing body of evidence has accumulated to support a cardio-protective effect of adenosine A3 receptor activation. This topic is well-addressed in another chapter in the book, only a brief summary will be described when relevant. [Pg.257]

Taken together, using a mouse model of hindlimb skeletal muscle injury, all three adenosine receptor subtypes could each individually induce protection from ischemia-reperfusion injury in skeletal muscle. Due to the lack of a highly selective A2B receptor agonist and antagonist, its role in mediating an anti-ischemic effect in skeletal muscle remains to be determined. [Pg.268]

Little is known regarding the effector mechanism of adenosine receptors in their protection against ischemia-reperfusion injury. In the pig latissimus dorsi muscle flap model, either glibenclamide or 5-hydroxydecanoate was able to reverse the... [Pg.269]

Oshima, K., Akao, T., Kobayashi, K., Muraoka, M., Matsumoto, K., Takeyoshi, I. The effect of direct hemoperfusion with a polymyxin B-immobilized fiber column (DHP-PMX therapy) on pulmonary ischemia-reperfusion injury in a canine model. J Invest Surg 21 (2008) 127-132. [Pg.337]

Protects against ischemia-reperfusion injury in an experimental model of controlled non-heartbeating donor kidney [174]... [Pg.261]

Studies in various animal models and in human hearts suggest that apoptosis does occur in ischemia/reperfusion injury of the heart, though the relative contribution of apoptosis in comparison with necrosis to cell loss in ischemia/ reperfusion injury is still controversial. Cardiomyocyte apoptosis was first reported by Gottlieb et al. [107], who studied the ischemia/reperfusion in rabbit hearts and found the hallmark of apoptosis in ischemic/reperfused hearts but not in the normal or ischemic-only rabbit hearts. Identification of apoptosis was based on the presence of fragmented DNA in electrophoretic gels, on in situ nick end-labeling assays, and on electron microscopy. They concluded that apoptosis may be a specific feature of reperfusion injury in cardiac myocytes. Subsequent studies have shown that apoptosis probably occurs both in ischemia and reperfusion [108], It appears that apoptosis is more prominent after ischemia followed by reperfusion than after ischemia alone [109, 110],... [Pg.20]

Studies Showing the Effect of Treatment with Caspase Inhibitors in Experimental Models of Ischemia/Reperfusion Injury to the Heart0... [Pg.29]

Renal ischemia/reperfusion injury in vivo activates caspase-1 and caspase-3 [62, 70]. In a murine model of ischemia/ reperfusion injury, ZVAD-fmk, a pancaspase inhibitor, was shown to attenuate reperfusion-induced DNA damage (as determined by TUNEL assay) and inflammation [65]. Down-regulation of caspase-3 and caspase-8 by siRNA provided protection from acute kidney injury in a mice model of ischemia-reperfusion injury (71). Recent studies by Edelstein et al. [66, 72] help estabhsh a hnk between the inflammatory aspects of the ischemic/reperfusion injury and caspase activation. In these studies it was observed that caspase 1 deficient mice were protected from ischemia-reperfusion... [Pg.160]

Burne MJ, Haq M, Matsuse H, Mohapatra S, Rabb H Genetic susceptibility to renal ischemia reperfusion injury revealed in a murine model.Transplantation 69 1023-1025, 2000... [Pg.207]

Different experimental techniques have been also used to investigate ischemia-reperfusion injury. Table 2. Experimental models of isolated hearts cannot consider the contribution of blood components or neurohormonal changes as this occurs in in vivo studies. However, these studies are able to dissect potential underlying mechanisms of the ischemic injury. The mode of perfusion (working heart vs Langendorff mode or constant flow vs constant pressure), the use of pacing, the composition of the perfusate and the end-points chosen to assess myocardial injury (arrhythmias, functional recovery... [Pg.59]

A close association has been described for IL-8 and other CXCRl/2 ligands in acute inflammation, including neutrophil-mediated inflammatory diseases such as ischemia-reperfusion injury, bacterial pneumonia, adult respiratory distress syndrome, and other infectious diseases. Neutralization of IL-8 in rabbits has shown dramatic protection in several models of neutrophil-mediated acute inflammation (261,262). [Pg.161]


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See also in sourсe #XX -- [ Pg.71 ]




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Animal models ischemia-reperfusion injury

Ischemia reperfusion

Reperfusion

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