Alpha-lipoic acid as a directly binding activator of the insulin receptor: protection from hepatocyte apoptosis.

Background And Aim: Alpha-lipoic acid has cytoprotective potential which has previously been explained by its antioxidant properties. The aim of this study was to assess LA-induced-specific cytoprotective signalling pathways in hepatocytes.

Methods: Apoptosis of rat hepatocytes was induced by actinomycinD/TNF-alpha.

Hepatocyte cytoskeleton during ischemia and reperfusion--influence of ANP-mediated p38 MAPK activation.

Aim: To determine functional consequences of this activation, whereby we focused on a potential regulation of the hepatocyte cytoskeleton during ischemia and reperfusion.

Methods: For in vivo experiments, animals received ANP (5 microg/kg) intravenously. In a different experimental setting, isolated rat livers were perfused with KH-buffer+/-ANP (200 nmol/L) +/-SB203580 (2 micromol/L).

Protein kinase A dependent signalling mediates anti-apoptotic effects of the atrial natriuretic peptide in ischemic livers.

Background/aims: Preconditioning of livers with atrial natriuretic peptide (ANP) attenuates ischemia-reperfusion injury (IRI) via the particulate guanylate cyclase. Recently, we have shown that ANP affects the p38 MAPK signalling cascade in the liver. Thus, aim of the present study was to elucidate the role of cGMP- and p38 MAPK-dependent signalling pathways in ANP-mediated anti-apoptotic effects.

Stimulation of p38 MAPK by hormonal preconditioning with atrial natriuretic peptide.

Aim: Stress-activated signaling pathways responsible for hepatic ischemia reperfusion injury and their modulation by protective interventions are widely unknown. Preconditioning of rat livers with Atrial Natriuretic Peptide (ANP) attenuates ischemia reperfusion injury (Gerbes et al. Hepatology 1998, 28:1309-1317).

Inhibition of p38 MAPK activation via induction of MKP-1: atrial natriuretic peptide reduces TNF-alpha-induced actin polymerization and endothelial permeability.

The atrial natriuretic peptide (ANP) is a cardiovascular hormone possessing antiinflammatory potential due to its inhibitory action on the production of inflammatory mediators, such as tumor necrosis factor-alpha (TNF-alpha). The aim of this study was to determine whether ANP is able to attenuate inflammatory effects of TNF-alpha on target cells. Human umbilical vein endothelial cells (HUVECs) were treated with TNF-alpha in the presence or absence of ANP.