Advertisement

Topics

PubMed Journals Articles About "Riociguat Prevents Hyperoxia Induced Lung Injury Pulmonary Hypertension" RSS

07:47 EDT 24th March 2019 | BioPortfolio

Riociguat Prevents Hyperoxia Induced Lung Injury Pulmonary Hypertension PubMed articles on BioPortfolio. Our PubMed references draw on over 21 million records from the medical literature. Here you can see the latest Riociguat Prevents Hyperoxia Induced Lung Injury Pulmonary Hypertension articles that have been published worldwide.

More Information about "Riociguat Prevents Hyperoxia Induced Lung Injury Pulmonary Hypertension" on BioPortfolio

We have published hundreds of Riociguat Prevents Hyperoxia Induced Lung Injury Pulmonary Hypertension news stories on BioPortfolio along with dozens of Riociguat Prevents Hyperoxia Induced Lung Injury Pulmonary Hypertension Clinical Trials and PubMed Articles about Riociguat Prevents Hyperoxia Induced Lung Injury Pulmonary Hypertension for you to read. In addition to the medical data, news and clinical trials, BioPortfolio also has a large collection of Riociguat Prevents Hyperoxia Induced Lung Injury Pulmonary Hypertension Companies in our database. You can also find out about relevant Riociguat Prevents Hyperoxia Induced Lung Injury Pulmonary Hypertension Drugs and Medications on this site too.

Showing "Riociguat prevents hyperoxia induced lung injury pulmonary hypertension" PubMed Articles 1–25 of 26,000+

Genipin attenuates hyperoxia-induced lung injury and pulmonary hypertension via targeting glycogen synthase kinase-3 β in neonatal rats.

Bronchopulmonary dysplasia is the most common chronic lung disease of infancy and is associated with pulmonary hypertension (PH). Inhibition of glycogen synthase kinase (GSK)-3 β has been shown to attenuate lung injury and PH in hyperoxia-exposed newborn rats. Genipin has been widely used for the treatment of inflammatory diseases. The aim of this study was to show that genipin decreased the expression of GSK-3 β in lung tissues of hyperoxia-exposed rat pups.


Reactive oxygen and nitrogen species induce cell apoptosis via a mitochondria-dependent pathway in hyperoxia lung injury.

Hyperoxia-induced lung injury limits the application of mechanical ventilation on rescuing the lives of premature infants and seriously ill and respiratory failure patients, and its mechanisms are not completely understood. In this article, we focused on the relationship between hyperoxia-induced lung injury and reactive oxygen species (ROS), reactive nitrogen species (RNS), mitochondria damage, as well as apoptosis in the pulmonary epithelial II cell line RLE-6TN. After exposure to hyperoxia, the cell viab...

Ginger ( Zingiber officinale ) prevents severe damage to the lungs due to hyperoxia and inflammation

Hyperoxia- and inflammation-induced lung injury is an important cause of the development of bronchopulmonary dysplasia (BPD) in premature infants. We aimed to ascertain the beneficial effects of ginger ( Zingiber officinale ) on rat pups exposed to hyperoxia and inflammation.


Caspase-1 Inhibition Attenuates Hyperoxia-Induced Lung and Brain Injury in Neonatal Mice.

Hyperoxia plays a key role in the development of bronchopulmonary dysplasia (BPD), a chronic lung disease of preterm infants. Infants with BPD often have brain injury that leads to long-term neurodevelopmental impairment, but the underlying mechanisms controlling BPD-induced neurodevelopmental impairment remain unclear. Our previous studies have shown that hyperoxia-induced BPD in rodents is associated with lung inflammasome activation. Here we tested the hypothesis that hyperoxia-induced lung and brain inj...

TREM-1 Attenuates RIPK3 Mediated Necroptosis in Hyperoxia Induced Lung Injury in Neonatal Mice.

Hyperoxia-induced injury to the developing lung, impaired alveolarization and dysregulated vascularization are critical factors in the pathogenesis of bronchopulmonary dysplasia (BPD); however, mechanisms for hyperoxia-induced development of BPD are not fully known. Here we show that the triggering receptor expressed on myeloid cells 1 (TREM-1) is upregulated in hyperoxia-exposed neonatal mice lungs as well as in tracheal aspirates (TA) and lungs of human neonates with respiratory distress syndrome (RDS) an...

Effect of heme oxygenase-1 on the apoptosis of type II alveolar epithelial cells in rats with hyperoxia-induced acute lung injury.

To investigate the effect of heme oxygenase-1 (HO-1) on the apoptosis of type II alveolar epithelial cells (AEC-II) in rats with hyperoxia-induced acute lung injury (HALI).

Oxymatrine prevents the development of monocrotaline-induced pulmonary hypertension via regulation of the N, N-dimethyl-L-arginine metabolism pathways in rats.

The purpose of this study was to investigate the potential effect of oxymatrine in monocrotaline-induced pulmonary hypertension and its possible influence on the N,N-dimethyl-L-arginine (ADMA) metabolism pathway. Pulmonary hypertension was induced in rats by a single-dose injection of monocrotaline (60mg/kg). Daily oral administration of oxymatrine (25, 50 and 100mg/kg) was started on the day following the monocrotaline injection for 28 days. Oxymatrine (50 and 100mg/kg) significantly attenuated monocrotali...

Lycium barbarum polysaccharide reduces hyperoxic acute lung injury in mice through Nrf2 pathway.

The disruption of the balance between antioxidants and oxidants plays a vital role in the pathogenesis of acute lung injury (ALI). Evidence has shown that Lycium barbarum polysaccharide (LBP) has antioxidant feature. We examined the efficacy and mechanisms of LBP on hyperoxia-induced acute lung injury (ALI) in the present study.

MicroRNA-34a Promotes Endothelial Dysfunction and Mitochondrial-Mediated Apoptosis in Murine Models of Acute Lung Injury.

Recent evidence has shown that microRNA (miRNAs) are involved in endothelial dysfunction and vascular injury in lung-related diseases. However, the potential role of miR-34a in the regulation of pulmonary endothelial dysfunction, vascular injury and endothelial cells (ECs) apoptosis in acute lung injury (ALI)/acute lung respiratory distress syndrome (ARDS) is largely unknown. Here, we show that miR-34a-5p was up-regulated in whole lungs, isolated ECs from lungs and ECs stimulated with various insults (lipop...

In this paper we have discussed epidemiology, pathogenesis, and approaches to treatment of chronic thromboembolic pulmonary hypertension (CTEPH). CTEPH is a unique potentially curable form of pulmonary hypertension. The gold standard of CTEPH treatment is pulmonary thromboendarterectomy. However, about 40% of patients with CTEPH are inoperable due to distal surgically inaccessible lesions of the pulmonary vasculature, severe hemodynamic impairments, or other contraindications. In addition, nearly half of pa...

Posttreatment With the Fatty Acid Amide Hydrolase Inhibitor URB937 Ameliorates One-Lung Ventilation-Induced Lung Injury in a Rabbit Model.

One-lung ventilation (OLV)-induced inflammation is a risk factor for acute lung injury that is responsible for 20% of postoperative pulmonary complications after lung resection. Inflammation is an important trigger for acute lung injury. Fatty acid amide hydrolase (FAAH) is the major enzyme that degrades the endocannabinoid arachidonoylethanolamine (AEA), an important regulator of inflammation, and its downstream metabolites such as arachidonic acid (AA) are also involved in inflammation. Importantly, AEA i...

VCAM-1-mediated neutrophil infiltration exacerbates ambient fine particle-induced lung injury.

Fine ambient particle matter (PM2.5) induces inflammatory lung injury; however, whether intratracheal administration of PM2.5 increases pulmonary polymorphonuclear leukocyte (PMN) infiltration, the mechanism of infiltration, and if these cells exacerbate PM2.5-induced lung injury are unknown.

Response to letter from dr Altmayer regarding publication "Sequential treatment with sildenafil and riociguat in patients with persistent or inoperable chronic thromboembolic pulmonary hypertension improves functional class and pulmonary hemodynamics".

Improvement of pulmonary arterial hypertension, inflammatory response, and epithelium injury by dual activation of cAMP/cGMP pathway in a rat model of monocrotaline-induced pulmonary hypertension.

Pulmonary hypertension (PH) is a life-threatening lung disease. PH with concomitant lung diseases, e.g., idiopathic pulmonary fibrosis, is associated with poor prognosis. Development of novel therapeutic vasodilators for treatment of these patients is a key imperative. We evaluated the efficacy of dual activation of cyclic adenosine monophosphate (cAMP) and cyclic guanosine monophosphate (cGMP) using an active, small-molecule phosphodiesterase (PDE4)/PDE5 dual inhibitor (Compound A). Compound A increased bo...

Perfusion Scintigraphy in Diagnosis and Management of Thromboembolic Pulmonary Hypertension.

Chronic thromboembolic pulmonary hypertension (CTEPH) is a life-threatening complication of acute pulmonary embolism (PE). Because the treatment of CTEPH is markedly different from that of other types of pulmonary hypertension, lung ventilation-perfusion (V/Q) scintigraphy is recommended for the workup of patients with unexplained pulmonary hypertension. Lung V/Q scintigraphy is superior to CT pulmonary angiography for detecting CTEPH. Perfusion defect findings of CTEPH can be different from those of acute ...

"Activation of Kv7 channels as a novel mechanism for NO/cGMP-induced pulmonary vasodilation".

The nitric oxide-NO/cGMP pathway represents a major physiological signalling controlling pulmonary arterial (PA) tone and drugs activating this pathway are used to treat pulmonary arterial hypertension. Kv channels expressed in PA smooth muscle cells (PASMC) are key determinants of vascular tone. We aimed to analyse the contribution of Kv1.5 and Kv7 channels in the electrophysiological and vasodilating effects evoked by NO donors and the GC stimulator riociguat in PA.

Monocrotaline pyrrole induces pulmonary endothelial damage through binding to and release from erythrocytes in lung during venous blood reoxygenation.

Monocrotaline has been widely used to establish an animal model of pulmonary hypertension, most frequently in rats. An important feature of this model resides in the selectivity of monocrotaline injury towards the pulmonary vascular endothelium versus the systemic vasculature when administrated at standard dosage. The toxic metabolite of monocrotaline, monocrotaline pyrrole, is transported by erythrocytes. This study aimed to reveal whether partial pressure of oxygen of blood determined the binding and rele...

Lung endothelial cell-targeted peptide-guided bFGF promotes the regeneration after radiation induced lung injury.

Basic fibroblast growth factor (bFGF) can protect the lung against radiation-induced pulmonary vascular endothelial apoptosis and subsequent radiation-induced lung injury (RILI). However, guiding bFGF to pulmonary vascular endothelial cells is a key determinant for the success of bFGF therapy. To improve the lung-targeting ability of bFGF, a lung endothelial cell-targeting peptide was fused to bFGF (LET-bFGF). An in vitro biological activity assay indicated that fusion of LET did not affect the bioactivity ...

Emerging role of extracellular vesicles in lung injury and inflammation.

Lung injury and inflammation are common characterizes in many pulmonary diseases. Alveolar epithelial cells, macrophages, pulmonary microvascular endothelial cells, and neutrophils, play crucial roles in lung injury and inflammation. They can secrete extracellular vesicles (EVs), involving exosomes, microvesicles, and apoptotic bodies. EVs are considered to be novel cell-cell communication tools, transferring diverse substances such as proteins, nucleic acid and lipids. Recently, the effects of EVs produced...

Neutrophils Disturb Pulmonary Microcirculation in Sepsis-induced Acute Lung Injury.

The lung is highly vulnerable during sepsis, yet its functional deterioration accompanied by disturbances in the pulmonary microcirculation are poorly understood. This study aimed to investigate how the pulmonary microcirculation is distorted in sepsis-induced acute lung injury (ALI) and reveal the underlying cellular pathophysiologic mechanism.Using a customized intravital lung microscopic imaging system in a murine model of sepsis-induced ALI, we achieved direct real-time visualization of the pulmonary mi...

Therapeutic effects of the selective farnesoid X receptor agonist obeticholic acid in a monocrotaline-induced pulmonary hypertension rat model.

Activation of the farnesoid X receptor (FXR), a member of the nuclear receptor steroid superfamily, leads to anti-inflammatory and anti-fibrotic effects in several tissues, including the lung. We have recently demonstrated a protective effect of the farnesoid X receptor (FXR) agonist obeticholic acid (OCA) in rat models of monocrotaline (MCT)-induced pulmonary arterial hypertension (PAH) and bleomycin-induced pulmonary fibrosis. The aim of the present study was to investigate whether the positive effects of...

Toll Like Receptor 4 Mediated Lymphocyte Imbalance Induces Nec-Induced Lung Injury.

Necrotizing enterocolitis (NEC) is the leading cause of death from gastrointestinal disease in premature infants, and is associated with the development of severe lung inflammation. The pathogenesis of NEC-induced lung injury remains unknown, yet infiltrating immune cells may play a role. In support of this possibility, we now show that NEC in mice and humans was associated with the development of profound lung injury that was characterized by an influx of Th17 cells and a reduction in Tregs. Importantly, t...

Intrauterine Growth Restriction and Hyperoxia as a Cause of White Matter Injury.

Intrauterine growth restriction (IUGR) is estimated to occur in 5% of pregnancies, with placental insufficiency being the most common cause in developed countries. While it is known that white matter injury occurs in premature infants, the extent of IUGR on white matter injury is less defined in term infants. We used a novel murine model that utilizes a thromboxane A2 (TXA2) analog (U46619), a potent vasoconstrictor, to induce maternal hypertension and mimic human placental insufficiency-induced IUGR to stu...

Ulinastatin protects rats from sepsis-induced acute lung injury by suppressing the JAK-STAT3 pathway.

Sepsis is usually accompanied by pulmonary inflammations, leading to acute lung injury. During this process, endogenous factors that play a regulatory role could be exploited to therapeutically alleviate such lethal tissue injury. Here, we showed that ulinastatin (UTI) administration could reduce lung tissue necrosis and swelling during sepsis in rats. UTI treatment also decreased the levels of inflammatory mediators both in the lung and in the serum. Mechanistically, we showed that the phosphorylation leve...

Prenatal exposure to pyrrolizidine alkaloids induced hepatotoxicity and pulmonary injury in fetal rats.

Hepatic and pulmonary toxicity in fetal rats induced by pyrrolizidine alkaloids (PAs) was investigated. Retrorsine (RTS) or monocrotaline (MCT) was intragastrically administered during pregnancy. The reduction of body and tail lengths was consistent with body weight loss in PA-exposed fetuses, and pathological lesions in liver and lung were observed only in fetuses. Both PAs reduced fetal serum transaminase activities. The GSH/GSSG ratio, GSH peroxidase and superoxide dismutase activities also decreased but...


Advertisement
Quick Search
Advertisement
Advertisement