[The effects of leptin on neuron apoptosis in mice with cerebral ischemia/reperfusion injury].

Objective: To study the effect of leptin on neuron apoptosis in mice with cerebral ischemia injury.

Methods: Seventy-five male Kuming mice were randomly divided into 3 groups:sham, model and leptin intervention group, respectively. Focal cerebral ischemia/reperfusion injury model in mice was established by middle cerebral artery occlusion.

[The effect of rosuvastatin therapy on CCR2 expression in mononuclear cells and its upstream pathway].

Objective: To investigate the effect of rosuvastatin therapy on C-C chemokine receptor(CCR2)expression in mononuclear cells in patients with carotid atherosclerosis and explore the possible upstream mechanism.

Methods: Twenty patients without previous statin treatment were enrolled. Rosuvastatin were given 5 to 20 mg/day for 3 months.

[Effect of repeated hypoxic preconditioning on renal ischemia-reperfusion-induced hepatic dysfunction in rats].

Objective: To explore the effect of repeated hypoxic preconditioning (RHP) on renal ischemia-reperfusion-induced hepatic dysfunction in rats and the underlying mechanism.

Methods: A total of 120 normal SD rats were randomly divided into 4 groups (n=40), namely RHP surgical group, RHP sham-operated (RHPS) group, nonhypoxic surgical group (IRI group), and nonhypoxic sham-operated group (S group). The rats in the hypoxic groups were exposed to hypoxia in a hypoxic chamber for 5 days prior to establishment of renal ischemia-reperfusion model by resection of the right kidney and clamping the left renal hilum.

Serum CRP and urinary trypsin inhibitor implicate postoperative cognitive dysfunction especially in elderly patients.

Purpose: Postoperative cognitive dysfunction (POCD) characterized as the decline of memory and executive function after major surgery is not well illustrated. The aim of this study is to discover whether inflammatory cytokines and urinary trypsin inhibitor (uTi) contribute to the development of POCD.

Method: Sixty-three patients undergoing lumber discectomy and 47 age-matched control volunteers were involved in this study.

Inhibition of the connexin 43 elevation may be involved in the neuroprotective activity of leptin against brain ischemic injury.

Leptin is a multifunctional hormone produced by the ob gene and is secreted by adipocytes that regulate food intake and energy metabolism. Numerous studies demonstrated that leptin is a novel neuroprotective effector, however, the mechanisms are largely unknown. Herein, we demonstrate the protective activities of leptin after ischemic stroke and provide the first evidence for the involvement of the connexin 43 (Cx43) in leptin-mediated neuroprotection.

Is leptin a predictive factor in patients with lung cancer?

Objectives: The aim of this study was to evaluate the expression and clinical significance of leptin in lung cancer.

Methods: 126 patients with lung cancer ranged from 30 to 83years of age were studied. Serum leptin levels were determined by ELISA.

Localized leptin release may be an important mechanism of curcumin action after acute ischemic injuries.

Background: Previous studies have demonstrated that both curcumin and leptin are protective factors against acute injuries. Here, we investigated whether leptin and its signaling pathway mediate the protective effects of curcumin.

Methods: A solid dispersion of curcumin-polyvinylpyrrolidone K30 was prepared and administered intraperitoneally.

[The effect of leptin on Cx43 expression in protecting mice cerebral ischemia/reperfusion injury].

Objective: To explore the effect of leptin on expression of Cx43 after rat cerebral ischemia/ reperfusion injury and its related mechanism.

Methods: Forty-five male kunming mice were randomly divided into 3 groups: sham group, model group and leptin group. Mouse models of transient focal cerebral ischemia were established by occlusion of the right middle cerebral artery for 2 h followed by 24 h reperfusion in model and leptin group.

Leptin administration alleviates ischemic brain injury in mice by reducing oxidative stress and subsequent neuronal apoptosis.

Background: Recent research has indicates that leptin plays a protective role in traumatic brain injury. We studied the protective effect of leptin on cerebral ischemia/reperfusion injury by using mice transient focal cerebral ischemia/reperfusion injury model.

Methods: The distribution of 125I-leptin in the mouse brain was assessed by radioimmunoassay method.

Leptin attenuates cerebral ischemia/reperfusion injury partially by CGRP expression.

Ischemic stroke is a medical emergency triggered by a rapid reduction in blood supply to localized portions of the brain, usually because of thrombosis or embolism, which leads to neuronal dysfunction and death in the affected brain areas. Leptin is generally considered to be a strong and quick stress mediator after injuries. However, whether and how peripherally administered leptin performs neuroprotective potency in cerebral stroke has not been fully investigated.

Leptin relieves intestinal ischemia/reperfusion injury by promoting ERK1/2 phosphorylation and the NO signaling pathway.

Background: Recently, research has indicated that leptin plays a protective role in traumatic brain and liver injury. We studied the protective effect of leptin on intestinal I/R injury and examined its mechanism by using mice intestinal I/R model and murine peritoneal macrophage hypoxia/reoxygenation (H/R) injury model.

Methods: Leptin was intraperitoneally administrated at 45 minutes after ischemia, then reperfusion for two hours.

[The role of Leptin on neuron apoptosis in mice with cerebral ischemia/reperfusion injury].

Objective: To study the effect of Leptin on neuron apoptosis in mice with cerebral ischemia injury and its mechanism.

Methods: Seventy-five mice were randomly divided into three groups. Focal cerebral ischemia/reperfusion injury model in mice was reproduced by middle cerebral artery occlusion for 2 hours followed by reperfusion.

A clinical study on the effects and mechanism of xuebijing injection in severe pneumonia patients.

Objective: To observe the effects of Xuebijing Injection in patients with severe pneumonia, and to explore the mechanism.

Methods: Eighty cases of severe pneumonia are randomly assigned to the Xuebijing treatment (forty cases) and the control group (forty cases), with the same routine therapy provided in both groups. Clinical effective rates, inflammatory factors and organ function were observed in both groups.

[Effect of inhibition of cytosolic phospholipase A₂ on Leptin release from human umbilical vein endothelial cells induced by lipopolysaccharide].

Objective: To determine Leptin levels in supernatant fluid of culture of human umbilical vein endothelial cells (ECV-304) after being challenged by lipopolysaccharide (LPS) and calcium ion vector A23187, and to explore the possible relation between Leptin release and cytosolic phospholipase A(2) (cPLA(2)) activity in an inflammatory cell model.

Methods: ECV-304 cells were cultured in vitro. Experiment 1: the cells were divided into seven groups: blank control group, LPS 5, 10, 20 μg/ml stimulation groups, A23187 0.

[Preliminary investigation of the changes and mechanism of Leptin after myocardial ischemia/reperfusion injury].

Objective: To explore the effect of rat myocardial ischemia/reperfusion (I/R) injury on serum Leptin, endothelin (ET), C-reactive protein (CRP) and myocardial Leptin expression, and discuss the role of Leptin in myocardial I/R injury.

Methods: Fifty Sprague-Dawley (SD) rats were randomly divided into sham-operation, ischemia and I/R 1, 2, 3 hours groups, with 10 rats in each group. Anterior descending artery of the left coronary artery was ligated for 45 minutes and released for 1, 2 and 3 hours to establish myocardial I/R model, and the said artery of the rats in sham-operation group was not ligated.

Endogenous leptin fluctuates in hepatic ischemia/reperfusion injury and represents a potential therapeutic target.

Aim: To evaluate the role of leptin in the internal disorders during hepatic ischemia/reperfusion injury.

Methods: A rat model of 70% hepatic ischemia/reperfusion injury was established, with groups of sham-operation (Sham), 60 min ischemia/60 min reperfusion (I60'R60'), I60'R150', I60'R240' and I60'R360'. Serum leptin was detected by a self-produced radioimmunoassay; serum glucose, total anti-oxidation capacity, myeloperoxidase, alanine transaminase and diamine oxidase were determined by relevant kits, while histological alterations and protein levels of leptin in the lung, liver and duodenum were examined by hematoxylin-eosin staining and immunohistochemistry.

[Effects of leptin on apoptosis of rat cerebral astrocytes with ischemia/hypoxia injury].

Objective: To investigate the effect of leptin on apoptosis of rat cerebral astrocytes with ischemia/ hypoxia injury and its mechanism.

Methods: The cerebral astrocytes with ischemic/hypoxia injury were induced in neonatal SD rats. The cellular viability of injury of astrocytes was detected by MTT assay.

[Role of leptin in hepatic ischemia/reperfusion-induced hepatic injury].

Unlabelled: OBJECTIVE; To study the changes of leptin after hepatic ischemia/reperfusion (H-I/R) and its effects on H-I/R-induced hepatic injury.

Methods: A 70% H-I/R model of rats was established. The rats were divided into groups with different reperfusion times and sham-operation group.

[Effects of ethyl pyruvate on injuries of sepsis in mice].

Objective: To explore the effect of ethyl pyruvate (EP) and alkaline phosphatase (ALP) on injuries of sepsis and the mechanism involved.

Methods: A murine sepsis model of cecal ligation and puncture was reproduced, and 90 male Kunming mice were divided randomly into sham-operation, model and EP-intervention groups. 75 mg/kg EP was intraperitoneally injected in EP groups 1 hour after establishment of model, and the mice in model group were given a same volume of Ringer's solution.

Heart-type fatty acid-binding protein is a useful marker for organ dysfunction and leptin alleviates sepsis-induced organ injuries by restraining its tissue levels.

Heart-type fatty acid-binding protein (H-FABP) is widely distributed and has been used to diagnose certain diseases. However, its alteration during infection-evoked organ dysfunction, and the potential association between leptin and it in injury or infection has not been investigated. In the current study, serum H-FABP, leptin, C-reactive protein and interleukin-1beta in the patients with pulmonary infection-induced multiple organ dysfunction were detected.

[Changes of leptin levels in serum and myocardium after myocardial ischemia/reperfusion injury].

Aim: To explore the effect of rat myocardial ischemia/reperfusion injury on leptin levels in serum and myocardium, and discuss the role of leptin in myocardial ischemia/reperfusion injury.

Methods: A myocardial ischemia/reperfusion injury model of rats was established, serum lactate dehydrogenase (LDH) and leptin levels were detected, and histopathological changes and leptin expressions in myocardium were investigated by hematoxylin-eosin staining and immunohistochemistry, respectively.

Results: Serum LDH of ischemia and reperfusion groups increased significantly (P < 0.

[Protective effect of leptin against cerebral ischemia/reperfusion injury in mice].

Objective: To investigate the protective effect of leptin against cerebral ischemia/reperfusion injury in mice.

Methods: Mouse models of transient focal cerebral ischemia were established by occlusion of the right middle cerebral artery for 2 h followed by 24 h reperfusion. The infarct volume and neurological deficit scores following leptin treatment were determined using TTC staining and the Longa's score, respectively, to evaluate the protective effect of leptin against ischemic cerebral injury.

[Distribution of leptin expression and its effect on the recovery of sepsis-induced internal disorders].

Objective: To explore the distribution of leptin expression and the effect of sepsis on leptin protein and mRNA levels.

Methods: Vital organ samples including hypothalamus, lung, liver, spleen, stomach, duodenum, kidney, epididymal fat pad and testis of normal rats were collected. The mRNA expressions of leptin in those samples were determined by RT-PCR.

[Effect of acute intra-peritoneal infection on leptin expression levels in peripheral blood and vital organs of rats].

Aim: To explore the effect of acute intra-peritoneal infection on leptin expression levels in peripheral blood and vital organs, and find out the role leptin plays in acute inflammation.

Methods: A cecal ligation and perforation model of rats was established, setting groups of sham-operation, intralipid injection, injury, estradiol injection and insulin injection. A rat leptin radioimmunoassay was used to check serum leptin concentrations at 12 h after the injury, and RT-PCR was also used to detect leptin mRNA expressions in adipose tissue, lung and liver.

Leptin protects vital organ functions after sepsis through recovering tissue myeloperoxidase activity: an anti-inflammatory role resonating with indomethacin.

In this research, the role of leptin on sepsis-induced organ dysfunction was evaluated. Making use of a mice sepsis model, changes of alanine transaminase and uric acid in serum, myeloperoxidase activity, leptin levels and histological alterations in heart, lung, liver and kidney were determined. Results showed that sepsis induced significantly higher levels of serum alanine transaminase and uric acid, decreased tissue myeloperoxidase activity and leptin levels, and triggered distinct histological alterations.