[Hydrogen sulfide reduces lipopolysaccharide-induced acute lung injury and inhibits expression of phosphorylated p38 MAPK in rats].

To investigate the influence of hydrogen sulfide (H₂S) on p38 MAPK signaling pathway during acute lung injury (ALI) caused by lipopolysaccharide (LPS), the rats were randomly divided into six groups: control group, LPS group, LPS + NaHS group, LPS + PPG (cystathionine-γ-lyase inhibitor) group, NaHS group and PPG group. The rats were sacrificed 6 h after injection and lung tissues were obtained. The structure of lung tissues and the number of polymorphonuclear leucocyte (PMN) was observed under optical microscope; the lung myeloperoxidase (MPO) activity, superoxide dismutase (SOD) activity and malondialdehyde (MDA) content were tested; intercellular adhesion molecule-1 (ICAM-1) protein expression changes were detected by immunohistochemical staining; phosphorylated p38 MAPK (p-p38 MAPK) protein expression was detected by Western blotting.

[Administration of hydrogen sulfide intraperitoneally reverses the hyporesponsiveness of rat pulmonary artery induced by lipopolysaccharide and its relationship with carbon monoxide].

Objective: To explore the effect of hydrogen sulfide (H(2)S) on abnormal pulmonary artery reactivity induced by lipopolysaccharide (LPS) and its relationship with carbon monoxide (CO).

Methods: Forty eight rats were divided into four groups randomly according to table of random number: control group (normal saline, NS), LPS group, a donor of H(2)S sodium hydrosulfide (NaHS)+LPS group, and NaHS+NS group (n=12 in each group). Rats were given LPS by intratracheal instillation (0.

[Effect of hydrogen sulfide on rat pulmonary artery reactivity and injury induced by lipopolysaccharide].

Objective: To explore the effects of hydrogen sulfide (H2S) on abnormal pulmonary artery reactivity and injury induced by lipopolysaccharide (LPS).

Methods: Seventy-two rats were divided into four groups randomly according to table of random number: control group, LPS group, sodium hydrosulfide (NaHS) as a donor of H2S+LPS group and NaHS+normal saline (NS) group (n=18 in each group). Rats were challenged with 0.

[The expression of cholecystokinin-octapeptide receptor in vascular endothelial cells induced by lipopolysaccharide].

Objective: To investigate the expression of cholecystokinin-octapeptide receptor (CCK-R) mRNA, and observe the effect of lipopolysaccharide (LPS) on CCK-AR mRNA and CCK-BR mRNA expression in ECV-304.

Methods: The human umbilical vein endothelial cell line ECV-304 was cultured and treated with LPS in dosage of 0.01, 0.

[Role of endogenous and exogenous hydrogen sulfide in acute lung injury induced by LPS in rats].

Aim: To explore the role of endogenous and exogenous hydrogen sulfide (H2S) in lipopolysaccharide (LPS)-induced acute lung injury (ALI) in rats and the underlying mechanisms.

Methods: 120 Sprague-Dawley rats were randomly divided into four groups: control, LPS (instilled intratracheally to induce ALI), NaHS (H2S donor) + LPS, and propargylglycin (PPG) + LPS. Animals were sacrificed at 4 h or 8 h after agent administration.

[Role of hydrogen sulfide/cystathionine-gamma-lyase system in acute lung injury induced by lipopolysaccharide in rats].

Objective: To explore the role of hydrogen sulfide/cystathionine-gamma-lyase (H(2)S/CSE) system in lipopolysaccharide (LPS)- induced acute lung injury (ALI) in rats and the underlying mechanisms.

Methods: Sixty-four Sprague-Dawley (SD) rats were randomly divided into four groups: control, LPS (instilled intratracheally to induce ALI), sodium hydrosulfide (NaHS), propargylglycine (PPG). Animals were sacrificed at 4 and 8 hours (n=8) after administration of the above agents.

[The role of hydrogen sulfide in acute lung injury during endotoxic shock and its relationship with nitric oxide and carbon monoxide].

Objective: To explore the role of hydrogen sulfide (H2S) in acute lung injury (ALI) during endotoxic shock (ES) and its relationship with nitric oxide (NO) and carbon monoxide (CO).

Methods: Sixty-four adult male SD rats were randomly divided into 4 equal groups: control group injected with normal saline via the caudal vein, lipopolysaccharide (LPS)-treated group injected with LPS to establish ES model, LPS + NaHS group injected with LPS and sodium hydrosulfide (NaHS, an exogenous H2S donor], and LPS + PPG group injected with LPS and polypropylene glycol (PPG, a H2S synthase inhibitor). The mean artery pressure (MAP) was measured via a polyethylene catheter in the right common carotid artery for 6 h.

[Effects of melatonin on anti-oxidative function of lung injury induced by lipopolysaccharide in rats and ICAM-1 expression].

Aim: To investigate the protective effect of melatonin (MT) on lung tissues during acute lung injury (ALI) in rats and its possible mechanism.

Methods: All rats were randomly divided into four groups: control group, lipopolysaccharide (LPS) group, dexamethasone (DEX) and MT treatment group. Myeloperoxidase (MPO) activity, superoxide dismutase (SOD) activity and malonaldehyde (MDA) content of lung tissues were detected at 3, 6 and 12 h after intratracheal instillation in each group.

[Inhibitory effect of melatonin on the expression of nuclear factor-kappaB during acute lung injury in rats].

Objective: To investigate the protective effect of melatonin (MT) on lung tissue during acute lung injury (ALI) in rats and its possible mechanism.

Methods: Ninety-six Sprague-Dawley (SD) rats were randomly divided into four groups: control group, lipopolysaccharide (LPS) group, dexamethasone (DEX) and MT treatment group, with 24 rats in each group. Rat model of ALI was established by instilling LPS intratracheally, and DEX and MT were injected intraperitoneally.

[The effect of puerarin on prevention of oxidative damage of cultured lens capsule epithelial cells].

Objective: To investigate the peroxynitrite damage to the lens epithelial cells (LEC) and the prevention of this damage by puerarin in vitro.

Methods: This paper was experimental study. Rabbit LEC were isolated and cultured and the third or forth passage LEC were used in this experiment The experiment groups included: (1) CONTROL GROUP: Heat-pathogen free saline (NS) 200 microl was added to the medium; (2) ONOO- group: ONOO- 200 microl was added to obtain the terminal concentration at 0.

[The protective function of puerarin to the injury of the lung and its mechanisms during diabetes].

Aim: To evaluate the roles of puerarin in alleviating the STZ-induced lung injury.

Methods: DM model was established by streptozotocin (STZ) intraperitoneal injection to study the injury mechanisms of the lung. SD rats were divided randomly into control group (C group), diabetes group (DM group), diabetes + puerarin group (DM + Pur group).

[Relationship between hydrogen sulfide and myocardial damage in endotoxemic rats].

To investigate the changes and role of hydrogen sulfide (H2S) in myocardial damage in endotoxemic rats, a rat model of endotoxemia induced by injection of lipopolysaccharide (LPS) was developed. Male Wistar rats were divided into four groups: control group, LPS group, LPS + propargylglycine (PPG, a metabolic enzyme inhibitor of H2S) group and LPS + NaHS (H2S donor) group. The mean arterial pressure (MAP) of rats within 4 h was observed, TNF-alpha and H2S contents in plasma, TNF-alpha and H2S contents, lactate dehydrogenase (LDH) and myeloperoxidase (MPO) activity in cardiac muscles were determined.

[Protective effect of endogenous carbon monoxide on organs during septic shock in rat and its mechanisms].

Objective: To study the protective effect of endogenous carbon monoxide (CO) on lung and liver during septic shock in rat and its mechanism.

Methods: Septic shock model was replicated by cecal ligation and puncture (CLP). Ninety-six rats were randomly divided into sham operation group, CLP group, CLP+ hemin (Hm) group and CLP+zinc protoporphyrin (ZnPP) group.

[Protective role of endogenous carbon monoxide to lung and kidney tissues during septic shock].

Aim: To study the protective role of endogenous carbon monoxide to lung and kidney tissues during septic shock and its mechanism.

Methods: A rat model of CLP was built by using the method of CLP. The malondialdehyde (MDA) content and the activity of superoxide dematase (SOD) in blood, lung and kidney were detected by immunohistochemical technique and light microscope.

Puerarin decreases lens epithelium cell apoptosis induced partly by peroxynitrite in diabetic rats.

The present study was designed to observe if puerarin decreases lens epithelium cell (LEC) apoptosis induced partly by peroxynitrite (ONOO(-)). One hundred and eight rats were randomly divided into control group (n=36), streptozotocin (STZ) group (n=36) and STZ + puerarin group (n=36). The rats in the control group intraperitoneally (i.

The antagonism of cholecystokinin octapeptide-8 to the peroxynitrite oxidation on a diabetic cataractal rat model.

Background: Cataracts is considered be formed because of an abnormal glucose metabolic pathway or oxidative stress. We explored the damaging role of ONOO- and antagonism of cholecystokinin octapeptide-8 (CCK-8) in diabetic cataractal rat lenses.

Methods: A diabetic cataractal animal model was established by peritoneal injection of streptozotocine (STZ).

[Effects and mechanisms of cholecystokinin octapeptide on hippocampal injury during endotoxic shock].

Aim: To study the effects and the mechanisms of cholecystokinin octapeptide(CCK-8) on hippocampal injury during endotoxic shock (ES).

Methods: Rabbits were injected intravenously with lipopolysaccharide (LPS, 8 mg/kg) to establish ES model. Thirty-two Rabbits were divided into 4 groups at random (n = 8): control (saline, iv), LPS, CCK-8 + LPS (CCK-8 pre-administrated 30 min before LPS, iv), proglumide (Pro, nonspecific antagonist of CCK receptors) + LPS (Pro pre-administrated 30 min before LPS, iv) group.

[Receptor mechanisms underlying the modulation of lipopolysaccharide-induced nuclear factor-kappaB expression in vascular endothelial cells by cholecystokinin octapeptide].

Objective: To elucidate the receptor mechanisms underlying the modulation of lipopolysaccharide (LPS)-induced nuclear factor-kappaB (NF-kappaB) expression in human umbilical vein endothelial cell line ECV-304 cells by cholecystokinin octapeptide (CCK-8).

Methods: Human umbilical vein endothelial cell line ECV-304 cells were stimulated with vehicle, LPS, CCK-8 (10(-9)-10(-7) mol/L), CCK receptor non-specific antagonist proglumide, CCK-A receptor (CCK-AR) specific antagonist CR-1409 or CCK-B receptor (CCK-BR) specific antagonist CR-2945 singularly or in combination. The NF-kappaB p65 protein level was determined by Western blot and immunocytochemistry technique.

[Inhibitory effect of cholecystokinin octapeptide on lipopolysaccharide-elicited inducible nitric oxide synthase expression in vascular endothelial cells].

Objective: To investigate the effect of cholecystokinin octapeptide (CCK-8) on lipopolysaccharide (LPS)-elicited inducible nitric oxide synthase (iNOS) expression in vascular endothelial cells.

Methods: Human umbilical vein endothelial cell line (ECV-304 cells) was stimulated with vehicle (normal saline) or LPS in the presence (0.01, 0.

Multiple factors contributing to lipopolysaccharide-induced reactivity changes in rabbit pulmonary artery.

To explore the underlying mechanism(s) of pulmonary arterial hypertension in endotoxic shock, the roles of N-acetylcysteine (NAC), nitric oxide (NO) and carbon monoxide (CO) were investigated. Pulmonary arterial rings (3-mm width) were prepared from 24 rabbits. Lipopolysaccharide (LPS), after 7-hour incubation, decreased the endothelium-dependent relaxation response of the arterial ring (pre-contracted with phenylephrine) to acetylcholine (1 mumol/L), but did not affect the endothelium-independent relaxation response to sodium nitroprusside.

[Effect of exogenous carbon monoxide on sequestration of polymorphonuclear neutrophils in the lung following limb ischemia-reperfusion: an experimental study].

Objective: To investigate the effect of exogenous carbon monoxide (CO) in inhibiting the sequestration of polymorphonuclear neutrophils (PMNs) in the lung following limb ischemia-reperfusion (IR) and the mechanism thereof.

Methods: PMNs of peripheral blood were isolated from the venous blood of a healthy volunteer. Serum was collected from a patient undergoing bilateral knee joint replacement as IR serum.

Effect of cholecystokinin octapeptide on diacylglycerol-PKC signaling pathway in rat pulmonary interstitial macrophages stimulated by lipopolysaccharide.

Aim: To investigate the effect of cholecystokinin octapeptide (CCK-8) on the diacylglycerol-protein kinase C (DAG-PKC) signaling pathway in rat pulmonary interstitial macrophages (PIM) stimulated by lipopolysaccaride (LPS).

Methods: The PIM from rat lung tissues were isolated using the collagenase digestion method combined with alveolar lavage and pulmonary vessel perfusion. DAG content and PKC activity were measured by radioenzymatic assay.

[Melatonin improves vascular reactivity of endotoxemia rats].

The purpose of the present study was to investigate the effect of melatonin (MT) on the abnormal reactivity of thoracic aorta and pulmonary artery induced by lipopolysaccharide (LPS) in rats. Sprague-Dawley rats were divided into four groups randomly: (1) Vehicle group; (2) LPS group: LPS (4 mg/kg, i.p.

Cholecystokinin octapeptide improves cardiac function by activating cholecystokinin octapeptide receptor in endotoxic shock rats.

Aim: To explore the effect of sulfated cholecystokinin octapeptide (sCCK-8) on cardiac functions and its receptor mechanism in endotoxic shock (ES) rats.

Methods: The changes of the mean arterial pressure (MAP), heart rate (HR), the left ventricular pressure (LVP) and the maximal/minimum rate of LVP (+/-LVdp/dt(max))) were measured by using physiological record instrument in eight groups of rats. The expression of cholecystokinin-A receptor (CCK-AR) and cholecystokinin-B receptor (CCK-BR) mRNA of myocardium in ES rats was examined by reverse transcription polymerase chain reaction (RT-PCR).

[Changes of HO-1 genes expression in liver following ischemia/reperfusion of limbs and their significance in rats].

Aim: To detect the changes of inducible heme oxygenase (HO-1) expression in liver following ischemia/reperfusion (I/R) of hindlimbs and to elucidate their significance.

Methods: I/R was established using the occlusion of the femoral arteries for 4h and reopening for 2-24 h in rats. The expression of HO-1 mRNA and HO-1 protein in liver tissue were detected with reverse transcription-polymerase chain reaction (RT-PCR) and immunohistochemical technique, respectively.