Role of Exogenous Hsp72 on Liver Dysfunction during Sepsis.

This study examined the role of exogenous heat shock protein 72 (Hsp72) in reversing sepsis-induced liver dysfunction. Sepsis was induced by cecal ligation and puncture. Liver function was determined on the basis of the enzymatic activities of serum glutamate oxaloacetate transaminase (GOT) and glutamate pyruvate transaminase (GPT).

Release of endogenous heat shock protein 72 on the survival of sepsis in rats.

Background: This study was undertaken to clarify the role of extracellular heat shock protein 72 on the survival of sepsis and to determine possible factor(s) that may be responsible for it.

Materials And Methods: Sepsis was induced by cecal ligation and puncture. Changes in serum levels of heat shock protein (Hsp72) and cytokines were determined during sepsis, and the results were correlated with the survival.

Nonlethal dose of silver nanoparticles attenuates TNF-α-induced hepatic epithelial cell death through HSP70 overexpression.

Silver nanoparticles (Ag-nps) have been widely used in various biomedical products. Compared with its hazardous effects extensively being studied, rare attention has been paid to the potential protective effect of Ag-nps to human health. The present study was designed to evaluate the protective effects of Ag-nps and heat shock treatment on tumor necrosis factor-α (TNF-α)-induced cell damage in Clone 9 cells.

Transcriptional Regulation of the Group IIA Secretory Phospholipase A2 Gene by C/EBP in Rat liver and its Relationship to Hepatic Gluconeogenesis during Sepsis.

Background: The present study was undertaken to test hypothesis that altered transcription of secretory Phospholipase A2 (sPLA2) gene in rat liver is regulated by CCAAT/enhancer binding protein δ (C/EBPδ), and to assess its relationship to hepatic gluconeogenesis during the progression of sepsis.

Methods: Sepsis was induced by Cecal Ligation and Puncture (CLP). Experiments were divided into three groups, control, early sepsis (9 h after CLP), and late sepsis (18 h after CLP).

Bioenergetic failure correlates with autophagy and apoptosis in rat liver following silver nanoparticle intraperitoneal administration.

Background: Deposition and accumulation of silver nanoparticles (Ag-nps) in the liver have been shown to induce hepatotoxicity in animal studies. The hepatotoxicity may include oxidative stress, abnormalities in energy metabolism, and cell death. Studies have indicated that autophagy is an intracellular event involving balance of energy, nutrients, and turnover of subcellular organelles.

Attenuation of mitochondrial unfolded protein response is associated with hepatic dysfunction in septic rats.

This study was conducted to reveal if the mitochondrial unfolded protein response (mtUPR), a conserved mitochondrial-nuclear communication mechanism, plays a critical role in the protein quality control system to cope with damaged protein during sepsis. Sepsis was induced by cecal ligation and puncture (CLP) in Sprague-Dawley rats. The efficiency of mtUPR was evaluated by measuring the transcriptional factors (CCAAT/enhancer-binder protein homologous protein [CHOP] and CCAAT/enhancer-binder protein-β) and chaperones (heat shock protein 60 [Hsp60] and Hsp10) expression in response to hepatic mitochondrial oxidized proteins (carbonylated proteins, car-proteins) and multi-ubiquitinated proteins (ub-proteins).

Changes in group II phospholipase A2 gene expression in rat heart during sepsis.

Background: This study was undertaken to investigate alterations of group II phospholipase A2 (PLA2) gene expression and its underlying mechanism in rat heart during different phases of sepsis.

Materials And Methods: Sepsis was induced by cecal ligation and puncture (CLP). Experiments were divided into three groups, control, early sepsis, and late sepsis.

Antisense inhibition of secretory and cytosolic phospholipase A2 reduces the mortality in rats with sepsis*.

Objective: Phospholipase A(2) has been implicated to play a pivotal role in the pathogenesis of sepsis syndrome. The two major forms of phospholipase A(2) isoenzymes, secretory phospholipase A(2) and cytosolic phospholipase A(2), are overexpressed during sepsis. The objective of this study was to test the hypothesis that inhibition of the overexpressed secretory phospholipase A(2) and cytosolic phospholipase A(2) during sepsis benefits the disease's eventual outcome.

Intracellular redistribution of dihydropyridine receptor in the rat heart during the progression of sepsis.

Background: Dihydropyridine receptor (DHPR) regulates the rate and force of cardiac muscle contraction. This study examined the alteration in the intracellular redistribution of DHPR and its association with the development of the two distinct cardiodynamic states in the rat heart during the progression of sepsis.

Material And Methods: Sepsis was induced by cecal ligation and puncture (CLP).

Transcriptional regulation of cardiac sarcoplasmic reticulum calcium-ATPase gene during the progression of sepsis.

Changes in sarcoplasmic reticulum Ca2+-ATPase (SERCA2a) gene expression in the rat heart during different phases of sepsis were studied. Sepsis was induced by cecal ligation and puncture (CLP). Septic rats were divided into two groups: the early hyperdynamic (9 h after CLP, early sepsis) and the late hypodynamic (18 h after CLP; late sepsis) groups.

G protein and adenylate cyclase complex-mediated signal transduction in the rat heart during sepsis.

Changes in the protein level of various subunits of GTP-binding protein and the activity of adenylate cyclase in the rat heart during different phases of sepsis were studied. Sepsis was induced by cecal ligation and puncture (CLP). Experiments were divided into three groups: control, early sepsis, and late sepsis.

Altered phospholamban-calcium ATPase interaction in cardiac sarcoplasmic reticulum during the progression of sepsis.

The purpose of this study was to investigate alterations of phospholamban phosphorylation and its interaction with Ca2+ transport(Ca2+-ATPase activity and Ca2+ uptake) in sarcoplasmic reticulum (SR) during the progression of sepsis. Sepsis was induced by cecal ligation and puncture (CLP). Phospholamban phosphorylation was studied by the labeling of the myocardial ATP pool by perfusing isolated rat hearts with [32P]H3PO4 followed by identification of the phosphorylated phospholamban.