Insulin protects against damage to pulmonary endothelial tight junctions after thermal injury: relationship with zonula occludens-1, F-actin, and AKT activity.

Intensive insulin therapy during critical illness protects the endothelium and thereby prevents organ failure. This study tested the hypothesis that insulin directly affects the attenuation of burn injury-induced damage to pulmonary endothelial tight junction and investigated the underlying mechanisms. Sprague Dawley rats with severe burn injury were randomized to treatment with insulin dissolved in normal saline (maintenance of blood glucose at a level between 5.

[Intensive insulin treatment protected the cardiac myocytes against apoptosis in severely scalded rats].

Objective: To investigate the effect of intensive insulin treatment, in the protection of myocardiocytes against apoptosis in severely scalded rats and its underlying mechanism.

Methods: Eighteen Sprague-Dawley (SD) rats were randomly divided into three groups (6/each) to receive: sham surgery, burn damage (on the back of the animals, degreeIII, to 30% of total body surface area), and burn damage+intensive insulin treatment. Tissue samples were collected from the left ventricle 6 hours after infliction of the burn damage for the examination of myocardial cell apoptosis [by terminal-deoxynucleotidyl transferase mediated nick end labeling (TUNEL) staining] and the expression of apoptosis-related molecules caspase-3, Bax, and Bcl-2 (by immuno-histochemistry and Western blotting).

Insulin-mediated inhibition of p38 mitogen-activated protein kinase protects cardiomyocytes in severe burns.

Thermal injury inhibits Akt activation and upregulates p38 mitogen-activated protein kinase, which in turn induces inflammation and increases apoptosis. This study aimed to elucidate the mechanism underlying the cytoprotective role of insulin in severe burns by examining the effects of insulin on inflammation and apoptosis mediated by p38 mitogen-activated protein kinase in burn serum-challenged cardiomyocytes. Neonatal rat cardiomyocytes were exposed to burn serum for 6 hours in the presence or absence of insulin and pretreated with inhibitors to p38 mitogen-activated protein kinase (SB203580) and Akt (LY294002).

Intensive insulin treatment attenuates burn-initiated acute lung injury in rats: role of the protective endothelium.

Nonmetabolic effects of intensive insulin therapy in critically ill patients have been reported, but the underlying mechanisms are unclear. This study was designed to test the hypothesis that intensive insulin treatment would attenuate burn-induced acute lung injury by protecting the pulmonary microvascular endothelium. The rat model of burn injury was achieved by exposure to 92°C water for 18 seconds.

[Effect of intensive insulin treatment on cardiac myocytes of severely scalded rats].

Objective: To study the protective effect of intensive insulin treatment on cardiac myocytes of severely scalded rats.

Methods: Eighteen model Sprague-Dawley (SD) rats were subjected to 30% total body surface area (TBSA) full thickness injury, and they were divided into three groups with 6 rats in each group. The right jugular vein was cannulated for fluid resuscitation and administration of drugs.

[Study on crosstalk between phosphatidylinositol 3 -kinase/Akt pathway and p38 mitogen-activated protein kinase pathway in cardiomyocyte with challenge of burn serum].

Objective: To investigate the possibility of crosstalk between phosphatidylinositol 3-kinase (PI3-K)/Akt pathway and p38 mitogen-activated protein kinase (p38MAPK) pathway in cardiomyocyte with challenge of burn serum, and to explore their influence on cardiomyocyte injury after burn.

Methods: The model of murine cardiomyocyte with stimulation of burn serum was established. (1) The level of Akt and p38 phosphorylation in cardiomyocyte were examined with stimulation of 10% burn serum before stimulation and 1, 3, 6, 12, 24 hour after stimulation.

[The anti-apoptosis effect of intensive insulin treatment on cardiac myocytes in severe scald rats].

Objective: To investigate the anti-apoptosis effect of intensive insulin treatment on cardiac myocytes and its underlying mechanism in severe scald rats.

Methods: Twelve SD rats were suffered from 30% TBSA full thickness scald, and they were divided into: IT group [with intravenous injection of isotonic saline including insulin (15 mU x kg(-1) x min(-1)) and 100 g/L glucose], B group [with treatment of isotonic saline (2 mL x kg(-1) x %TBSA(-1) x 8 h(-1)]. Six SD rats received sham burn as controls[sham(S)group, with treatment of fluid at physiologic dose].

[Protective effect of insulin on oxygen-radical induced hepatic injury in severely scalded rats].

Objective: To investigate the protective effect of insulin on oxygen-radical induced hepatic injury in severely scalded rats in early stage of severe scald.

Methods: Eighty-four male Sprague-Dawley rats were randomly divided into three groups: i. e, normal group, saline group, and insulin group, with 28 rat in each group.

[The protective effect of intensive insulin treatment on the myocardium in severely scalded rats].

Objective: To study the protective effect of intensive insulin treatment on the myocardium of severely scalded rats, and to primarily explore its mechanism.

Methods: Eighteen SD rats were divided into three groups, with 6 rats in each group. The rats in burn and intensive insulin group were inflicted with 30% TBSA full-thickness injury on the back.

[Study of the anti-endotoxin effect of beta-1, 2, 3, 4, 6-penta-O-galloyl-D-glucopyranose in vitro].

Objective: To study the anti-endotoxin effect of beta-1, 2, 3, 4, 6-penta-O-galloyl-D-glucopyranose (PGG) in vitro.

Methods: The affinity of PGG with lipid A was determined with biosensor technology, and the endotoxin-neutralizing effect was assayed with LAL. Human peripheral blood mononuclear cells (hPBMC) were separated from healthy donors and cultured in vitro.

[Experimental study on the antagonistic activity of cationic multi-peptide mastoparan-1 against lipopolysaccharide].

Objective: To explore the mechanism of cationic multi-peptide mastoparan-1 (MP-1) on the protection of mice from lipopolysaccharide (LPS) challenge.

Methods: Thirty Kunming mice were divided randomly into MP-1, injury, protection groups with 10 mice in each group. The mice in MP-1 group were injected with 3 mg/kg MP-1 by tail vein, while those in injury group were injected with 20 mg/kg LPS by tail vein, and those in protection group 3 mg/kg MP-1 within 20 seconds after 20 mg/kg LPS injection were injected.

[Study on the injurious effect of a self designed micro-skin machine on the epithelia].

Objective: To observe the injury on micro-skin induced by a self designed micro-skin machine.

Methods: Micro-skin was produced either with the machine or by hand. Cells at the edge of micro-skin were observed by transmission electron microscope.