Protective Effects of Mesenchymal Stem Cells Against Central Nervous System Injury in Heat Stroke.

Background: Heatstroke (HS) is a serious disease caused by central nervous system (CNS) injuries, such as delirium, convulsion, and coma. Currently, mesenchymal stem cells (MSCs) have demonstrated novel neuroprotective effects; therefore, this research explores the neuroprotective effects and mechanisms of MSCs against HS injury.

Methods: HS rat models were induced in a 40°C and 65% humidity environment until the rectal temperature reached 42°C.

Role of ultrasonographic features and quantified BRAFV600E mutation in lymph node metastasis in Chinese patients with papillary thyroid carcinoma.

The association between cervical lymph node metastasis (LNM) and ultrasonographic features as well as BRAF mutations in patients with papillary thyroid carcinoma (PTC) remained controversial. This study investigated the association between LNM and ultrasonographic features as well as BRAF mutation in Chinese patients with PTC. A total of 280 patients with PTC in China were included in this study.

[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.

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.

[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.

[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.