Cobalt protoporphyrin protects the liver against apoptosis in rats of brain death.

Brain death (BD) leads to a marked increase in apoptosis, which influences the viability of donor organs. Induction of heme oxygenase 1 (HO-1) has been shown to exert beneficial effects in different liver injury models. Therefore, we examined the effect of pretreating rats with cobalt protoporphyrin (CoPP), an HO-1 inducer, on apoptosis in liver during BD and elucidated the mechanisms involved.

Methylation of promoter and expression silencing of GPX3 gene in hepatocellular carcinoma tissue.

Background/aims: Accumulating evidence has identified transcriptional silencing by aberrant methylation of CpG islands as a potential mechanism for the inactivation of tumor suppressor genes. The role of aberrant methylation of the GPX3 promoter in hepatocellular carcinoma (HCC) is not yet clear. We investigated the association of the status of GPX3 promoter methylation and GPX3 protein expression with the clinicopathological progression of HCC.

Protective effects of SP600125 in brain death-induced liver injury.

The aim of the present study was to investigate the protective effect of SP600125, a selective c-Jun N-terminal kinase inhibitor, in brain death-induced liver injury. All 40 Sprague-Dawley rats are anesthetized. Analysis of liver histology, function, JNK phosphorylation status, as well as apoptosis related protein was evaluated in this study.

Modified brain death model for rats.

Objectives: Experimental animal models of brain death that mimic human conditions may be useful for investigating novel strategies that increase quality and quantity of organs for transplant.

Materials And Methods: Brain death was induced by increasing intracranial pressure by inflating an intracranial placed balloon catheter. Brain death was confirmed by flatline electroencephalogram, physical signs of apnea, and absence of brain stem reflexes.

Liver sinusoidal endothelial cell lectin, LSECtin, negatively regulates hepatic T-cell immune response.

Background & Aims: The liver is an organ with paradoxic immunologic properties and is known for its tolerant microenvironment, which holds important implications for hepatic diseases. The molecular basis for this local immune suppression, however, is poorly understood. In this study, we aimed to determine the role of liver sinusoidal endothelial cell lectin (LSECtin), a recently identified member of the dendritic cell-specific ICAM-3 grabbing nonintegrin (DC-SIGN) family, in the regulation of hepatic T-cell immune response.