[Expression of nucleolin in pressure overload-induced cardiac hypertrophy rats].

Objective: To detect the expression of nucleolin in cardiac hypertrophy rats induced by pressure overload.

Methods: A total of 40 SD rats with body weight 180 g and 220 g were recruited and randomly divided into 2 groups: a transverse aortic constriction (TAC) group and a sham surgery group. Cardiac hypertrophy model was employed by transverse aortic constriction surgery.

Nucleolin protects the heart from ischaemia-reperfusion injury by up-regulating heat shock protein 32.

Aims: Nucleolin plays important roles in a variety of cellular processes. In this study, we aimed to investigate the role of nucleolin in cardiac ischaemia-reperfusion (I-R) injury.

Methods And Results: We investigated the expression pattern of nucleolin in hearts subjected to I-R, or neonatal rat cardiomyocytes subjected to hypoxia-re-oxygenation.

Severe multiple organ injury in HSF1 knockout mice induced by lipopolysaccharide is associated with an increase in neutrophil infiltration and surface expression of adhesion molecules.

We have reported previously that HSF1 is essential in protection against the lethal systemic inflammation induced by LPS. However, the mechanism by which HSF1 protects against LPS-induced systemic inflammation remains unknown. In this study, HSF1(-/-) mice were subjected to endotoxemia by a bolus injection of LPS (10 mg/kg, i.

Increased stability of Bcl-2 in HSP70-mediated protection against apoptosis induced by oxidative stress.

We have previously shown that heat shock protein 70 (HSP70) markedly inhibits H(2)O(2)-induced apoptosis in mouse C2C12 myogenic cells by reducing the release of Smac. However, the molecular mechanism by which HSP70 interferes with Smac release during oxidative stress-induced apoptosis is not understood. In the current study, we showed that HSP70 increased the stability of Bcl-2 during oxidative stress.

WITHDRAWN BY AUTHOR: Heat shock protein 70 interacts with nucleolin and inhibits its cleavage, down-regulation and apoptosis induced by hydrogen peroxide in myocytes.

This manuscript has been withdrawn by the author.

Nucleolin/C23 mediates the antiapoptotic effect of heat shock protein 70 during oxidative stress.

Although heat shock protein 70 (Hsp70) has been shown to markedly inhibit H(2)O(2)-induced apoptosis in C2C12 cells, and nucleolin/C23 has also been implicated in apoptosis, the relationship of these two molecules is still largely unknown. The aim of the current study was to investigate the potential involvement of nucleolin/C23 in the antiapoptotic mechanism of Hsp70. We found that primary cultures of neonatal rat cardiomyocytes underwent apoptosis upon H(2)O(2) treatment, and in these cells nucleolin/C23 protein was highly unstable and had a half-life of less than 4 h.

KLF4 is a novel regulator of the constitutively expressed HSP90.

Krüppel-like factor 4 (KLF4) is a zinc finger-containing transcription factor with diverse regulatory functions in cell growth, proliferation, and differentiation. But little is known about the regulation of KLF4 on the expression of HSP90 (HSP84 and HSP86). In the current study, overexpression of KLF4 was firstly identified to promote the basal expression of HSP90 (HSP84 and HSP86) but not the inducible expression in the C2C12 cells and RAW264.

Effects of dobutamine on gut mucosal nitric oxide production during endotoxic shock in rabbits.

Background: Dobutamine is the agent of choice for increasing cardiac output during myocardial depression in humans with septic shock. Studies have shown that beta-adrenoceptor agonists influence nitric oxide generation, probably by modulating cyclic adenosine monophosphate. We investigated the effects of dobutamine on the systemic and luminal gut release of nitric oxide during endotoxic shock in rabbits.

The inhibition of LPS-induced production of inflammatory cytokines by HSP70 involves inactivation of the NF-kappaB pathway but not the MAPK pathways.

The objective of this study was to evaluate the negative regulatory role of heat shock protein 70 (HSP70) on endotoxin-induced activation of inflammatory cytokine signaling pathways in a macrophage cell line. Our studies show that elevation of HSP70 either by activation of the heat shock response (HSR) or through forced expression of the hsp70.1 gene downregulates cytokine expression.

Blood warming during hemofiltration can improve hemodynamics and outcome in ovine septic shock.

Background: This study was designed to evaluate the effects of blood warming during hemofiltration on global and regional hemodynamics, plasma lactate, and 24-h survival during septic shock.

Methods: Twenty anesthetized and mechanically ventilated sheep underwent induction of peritonitis and, 4 h later, were treated by hemofiltration with (n = 10) or without (n = 10) blood warming.

Results: In the group without blood warming, body temperature decreased after starting hemofiltration and remained below baseline.

[Oxidative stress-induced accumulation of heat shock protein 70 within nucleolus].

Objective: To investigate the effect of oxidative stress on the accumulation of heat shock protein 70 (HSP70) within C2C12 myogenic cells.

Methods: Heat shock response (42 degrees C for 1 h and recovery for 12 h at 37 degrees C) was used to induce the expression of heat shock protein 70. We constructed a recombinant plasmid of HSP70 with enhanced green fluorescent protein (EGFP).

[Roles of nuclear factor-kappaB in heat shock pretreatment to abate cardiomyocyte injury induced by hydrogen peroxide].

Objective: To investigate the role of nuclear factor-kappaB (NF-kappaB) in heat shock pretreatment to abate cardiomyocyte injury induced by hydrogen peroxide (H(2)O(2)).

Methods: The primary generation of cultured neonatal rat cardiomyocytes were injured by exposure to 1 mmol/L H(2)O(2) for different durations. The total antioxidant in cardiomyocytes was detected.

[Comparison of dobutamine under different fluids resuscitation for shock induced by ischemia/reperfusion].

Objective: To compare the effects of dobutamine under different fluids resuscitation for shock induced by intestinal ischemia/reperfusion (I/R) injury in rabbits.

Methods: Thirty-two anesthetized rabbits were randomized into four groups of eight animals each. The groups were followed as: (1) lactated Ringer's solution (LRS) resuscitation; (2) LRS+hydroxyethyl starch solution (HES) resuscitation; (3) LRS resuscitation+dobutamine treatment; (4) LRS+HES resuscitation+dobutamine treatment.

[Roles of hydroxyethyl starch solution in resuscitation for shock induced by ischemia/reperfusion injury of the intestine].

Objective: To compare the effects of high and low doses of 6% hydroxyethyl starch solution (HES) on resuscitation for shock induced by ischemia/reperfusion injury of the intestine in rabbits.

Methods: Thirty-two anesthetized rabbits were randomized into four groups of eight animals each. The animals in the control group received no fluid resuscitation, animals in group 2 received lactated Ringer's solution (LRS, 20 ml x kg(-1) x h(-1)), those in group 3 received LRS+HES (LRS 18 ml x kg(-1) x h(1)+HES 2 ml x kg(-1) x h(-1), low dosage of HES), and those in group 4 received HES only in high dosage of HES (20 ml x kg(-1) x h(-1)).

Gut mucosal damage during endotoxic shock is due to mechanisms other than gut ischemia.

Whether the gut alterations seen during sepsis are caused by microcirculatory hypoxia or disturbances in cellular metabolic pathways associated with mitochondrial respiration remains controversial. We hypothesized that hypoperfusion or hypoxia and local production of nitric oxide might play an important role in the development of gut mucosal injury during endotoxic shock and investigated their roles by using differing levels of fluid resuscitation and occlusion of the superior mesenteric artery (SMA). Anesthetized New Zealand rabbits were allocated to group I (sham, n = 8); group II [low-dose endotoxin (LPS, Escherichia coli-055:B5, 150 microg/kg)/fluid resuscitation (12 ml x kg(-1) x h(-1)); n = 8]; group III [high-dose LPS (1 mg/kg)/fluid resuscitation (12 ml x kg(-1) x h(-1)); n = 8]; group IV [high-dose LPS (1 mg/kg)/hypovolemia (4 ml x kg-1 x h(-1) fluids); n = 8]; and group V [SMA ligation/fluid resuscitation (12 ml x kg(-1) x h(-1)); n = 4].

Low-dose vasopressin in the treatment of septic shock in sheep.

After induction of cecal perforation, 20 anesthetized sheep were randomized to be treated, when arterial blood pressure fell below 75 mm Hg, with vasopressin (fixed dose of 0.02 U/minute), norepinephrine (0.5-5 microg/kg/minute titrated to maintain mean arterial pressure between 75 and 85 mm Hg), vasopressin + norepinephrine (vasopressin at fixed dose 0.

Optimal adrenergic support in septic shock due to peritonitis.

Background: The authors evaluated optimal adrenergic support using norepinephrine, dopamine, and dobutamine in a clinically relevant model of septic shock.

Methods: Twenty-eight mature, female, anesthetized sheep (weight, 30.5 +/- 3.