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PubMed Journals Articles About "Inhibition PHGDH Attenuates Bleomycin Induced Pulmonary Fibrosis" RSS

17:13 EDT 21st September 2018 | BioPortfolio

Inhibition PHGDH Attenuates Bleomycin Induced Pulmonary Fibrosis PubMed articles on BioPortfolio. Our PubMed references draw on over 21 million records from the medical literature. Here you can see the latest Inhibition PHGDH Attenuates Bleomycin Induced Pulmonary Fibrosis articles that have been published worldwide.

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Showing "Inhibition PHGDH Attenuates Bleomycin induced Pulmonary Fibrosis" PubMed Articles 1–25 of 23,000+

Inhibition of mTOR ameliorated bleomycin-induced pulmonary fibrosis by regulating epithelial-mesenchymal transition.

Epithelial-mesenchymal transition (EMT) plays a pivotal role in idiopathic pulmonary fibrosis (IPF). In bleomycin-induced pulmonary fibrosis mice, we observed that inhibition of mTOR (mammalia target of rapamycin) attenuated IPF. Rapamycin suppressed the down-regulation of E-cadherin and up-regulation of fibronectin in bleomycin-induced pulmonary fibrosis mice. In addition, dual immunofluorescence staining for E-cadherin and fibronectin demonstrated that rapamycin pretreatment decreased the proportions of A...


Dihydroartemisinin alleviates oxidative stress in bleomycin-induced pulmonary fibrosis.

Dihydroartemisinin has been shown to inhibit the development of pulmonary fibrosis in rats, but its mechanism has yet to be elucidated. This study aimed to determine the mechanisms of dihydroartemisinin in bleomycin-induced pulmonary fibrosis in a rat model.

MK2 Inhibition Attenuates Fibroblast Invasion and Severe Lung Fibrosis.

Severe pulmonary fibrosis such as idiopathic pulmonary fibrosis (IPF) is characterized by the accumulation of extracellular matrix and fibroblast activation. Targeting fibroblast activation has contributed to the development of anti-fibrotic therapeutics for patients with IPF. Mitogen-activated protein kinase-activated protein kinase 2 (MAPKAPK2, MK2), downstream in the TGF-β/p38MAPK pathway, has been implicated in inflammatory and fibrosing diseases. Increased levels of activated MK2 were expressed in IPF...


SIS3, a specific inhibitor of smad3, attenuates bleomycin-induced pulmonary fibrosis in mice.

Pulmonary fibrosis (PF) is a fatal respiratory disease with no effective medical treatments available. TGF-β/Smads signaling has been implicated to play an essential in the pathogenesis of PF, in which Smad3 act as the integrator of pro-fibrosis signals. In this study, we determined the effect of SIS3, a specific inhibitor of Smad3, in an experimental mouse model of lung fibrosis. We observed that SIS3 treatment significantly reduced bleomycin (BLM)-induced pathological changes and collagen deposition in t...

Pulmonary delivery of polyplexes for combined PAI-1 gene silencing and CXCR4 inhibition to treat lung fibrosis.

This report describes the development of polyplexes based on CXCR4-inhibiting poly(ethylenimine) derivative (PEI-C) for pulmonary delivery of siRNA to silence plasminogen activator inhibitor-1 (siPAI-1) as a new combination treatment of pulmonary fibrosis (PF). Safety and delivery efficacy of the PEI-C/siPAI-1 polyplexes was investigated in vitro in primary lung fibroblasts isolated from mice with bleomycin-induced PF. Biodistribution analysis following intratracheal administration of fluorescently labeled ...

Toll-like receptor expression in pulmonary sensory neurons in the bleomycin-induced fibrosis model.

Airway sensory nerves are known to express several receptors and channels that are activated by exogenous and endogenous mediators that cause coughing. Toll-like receptor (TLR) s are expressed in nociceptive neurons and play an important role in neuroinflammation. However, there have been very few studies of TLR expression in lung-derived sensory neurons or their relevance to respiratory symptoms such as cough. We used the bleomycin-induced pulmonary fibrosis model to investigate the change in TLR expressio...

Fructose-1,6-Bisphosphate Prevents Bleomycin-Induced Pulmonary Fibrosis in Mice and Inhibits the Proliferation of Lung Fibroblasts.

Pulmonary fibrosis is a specific form of interstitial pneumonia. In addition to the idiopathic cause, it may be caused by drugs such as bleomycin (BLM)-used in the treatment of tumors. Fructose-1,6-bisphosphate (FBP) is a high-energy endogenous glycolytic compound that has antifibrotic, anti-inflammatory, and immunomodulatory effects. The aim of this study was to investigate the effects of FBP on both BLM-induced pulmonary fibrosis in mice and in a human embryonic lung fibroblast (MRC-5) culture system. C57...

Astragaloside IV modulates TGF-β1-dependent epithelial-mesenchymal transition in bleomycin-induced pulmonary fibrosis.

Epithelial-mesenchymal transition (EMT) plays an important role in idiopathic pulmonary fibrosis (IPF). Astragaloside IV (ASV), a natural saponin from astragalus membranaceus, has shown anti-fibrotic property in bleomycin (BLM)-induced pulmonary fibrosis. The current study was undertaken to determine whether EMT was involved in the beneficial of ASV against BLM-induced pulmonary fibrosis and to elucidate its potential mechanism. As expected, in BLM-induced IPF, ASV exerted protective effects on pulmonary fi...

Fine mapping of the major bleomycin-induced pulmonary fibrosis susceptibility locus in mice.

Susceptibility to fibrotic lung disease differs among people and among inbred strains of mice exposed to bleomycin where C57BL/6J mice are susceptible and C3H/HeJ mice are spared fibrotic disease. Genetic mapping studies completed in offspring derived from these inbred strains revealed the inheritance of C57BL/6J alleles at loci, including the major locus on chromosome 17, called Blmpf1 bleomycin-induced pulmonary fibrosis 1, to be linked to pulmonary fibrosis in treated mice. In the present study, to reduc...

Use of human amniotic epithelial cells in mouse models of bleomycin-induced lung fibrosis: A systematic review and meta-analysis.

Idiopathic pulmonary fibrosis (IPF) urgently requires effective treatment. Bleomycin-induced lung injury models are characterized by initial inflammation and secondary fibrosis, consistent with the pathological features of IPF. Human amniotic epithelial cells (hAECs) exhibit good differentiation potential and paracrine activity and are thus ideal for cell-based clinical therapies. The therapeutic effects of hAECs on lung fibrosis are attributed to many factors. We performed a systematic review of preclinica...

Octreotide ameliorates dermal fibrosis in bleomycin-induced scleroderma

Insulin-like growth factor (IGF)-I is a differentiation and growth factor. Antifibrotic action of octreotide has been reported in pulmonary fibrosis. The present study aimed to research the prophylactic and therapeutic potential of octreotide on a bleomycin (BLM)-induced experimental scleroderma model.

Quercetin ameliorates pulmonary fibrosis by inhibiting SphK1/S1P signaling.

Idiopathic pulmonary fibrosis (IPF) is an agnogenic chronic disorder with high morbidity and low survival rate. Quercetin is a flavonoid found in a variety of herbs with anti-fibrosis function. In this study, bleomycin was employed to induce a pulmonary fibrosis mouse model. The quercetin administration ameliorated bleomycin-induced pulmonary fibrosis, evidenced by the expression level changes of hydroxyproline, fibronectin, α-smooth muscle actin, Collagen I and Collagen III. The similar results were obser...

Sinapic acid ameliorates bleomycin-induced lung fibrosis in rats.

Pulmonary fibrosis is a multifaceted disease with high mortality and morbidity, and it is commonly nonresponsive to conventional therapy.

Cangrelor alleviates pulmonary fibrosis by inhibiting GPR17-mediated inflammation in mice.

Pulmonary fibrosis is a progressive and intractable lung disease. Macrophages play a critical role in the progression of pulmonary fibrosis. Cangrelor, an anti-platelet agent, is also a non-selective Gprotein-coupled receptor 17 (GPR17) antagonist. GPR17 mediates microglial inflammation in the chronic phase of cerebral ischemia and regulates allergic pulmonary inflammation. In this study, we observed the effects of cangrelor on bleomycin (BLM)-induced macrophage cellular inflammation and BLM-induced pulmona...

Quercetin Enhances Ligand-induced Apoptosis in Senescent IPF Fibroblasts and Reduces Lung Fibrosis In Vivo.

While cellular senescence may be a protective mechanism in modulating proliferative capacity, fibroblast senescence is now recognized as a key pathogenic mechanism in Idiopathic Pulmonary Fibrosis (IPF). In aged mice, abundance and persistence of apoptosis-resistant senescent fibroblasts play a central role in non-resolving lung fibrosis after bleomycin challenge. Therefore, we investigated whether quercetin can restore the susceptibility of senescent IPF fibroblasts to pro-apoptotic stimuli and mitigate bl...

Hot topics from the Assemblies.

Tissue-resident alveolar macrophages (TR-AM) are depleted from the lung during the early stages of bleomycin-induced lung injury and fibrosis. The recovery of the population of macrophages after bleomycin could be completely attributable to the recruitment and differentiation of monocyte-derived alveolar macrophages (Mo-AM). The authors used multiple lineage-trace mouse models where they selectively depleted TR-AM or Mo-AM and induced fibrosis with bleomycin. Deletion of TR-AM had no effect on the severity ...

Synthesis and discovery of a drug candidate for treatment of idiopathic pulmonary fibrosis through inhibition of TGF-β1 pathway.

In this study, anti-IPF lead compounds 42 and 44, derived from natural sesquiterpene lactones Isoalantolactone and alantolactone, were discovered by screening from a high-throughput TGF-β1 reporter luciferase assay. Notably, they could reduce the myofibroblast activation and extracellular matrix deposition both in vitro and in vivo. Additionally, compounds 42 and 44 could significantly attenuate bleomycin-induced pulmonary fibrosis in mice. Further validation of pharmacokinetics study and toxicity evalua...

Submicron emulsion of cinnamaldehyde ameliorates bleomycin-induced idiopathic pulmonary fibrosis via inhibition of inflammation, oxidative stress and epithelial-mesenchymal transition.

Idiopathic pulmonary fibrosis (IPF) is the most frequent and severe form of idiopathic interstitial pneumonias. The pathogenesis is associated with inflammation and oxidative stress and epithelial-mesenchymal transition (EMT). Cinnamaldehyde exhibits antiinflammatory and antioxidant properties, but its effect on IPF is unknown. The present study is to investigate the anti-fibrotic effect and action mechanism of cinnamaldehyde on IPF.

Apixaban attenuates ischemia-induced myocardial fibrosis by inhibition of Gq/PKC signaling.

It was previously found that patients with symptom of myocardial dysfunction had increased levels of thrombin. Apixaban is one of the novel oral anticoagulant drugs widely used in clinic. As the inhibitor of FXa (prothrombin), it inhibits prothrombin conversion into thrombin leading to thrombin deficiency in vivo. However, the effects of apixaban on myocardial fibrosis were still unclear, and the concomitant molecular mechanisms remain to be investigated. Here, we showed that myocardial fibrosis-bearing mic...

Haplodeletion of Follistatin-like 1 Attenuates Radiation-induced Pulmonary Fibrosis in Mice.

Radiation-induced pulmonary fibrosis (RIPF) is a severe and life-threatening complication of radiotherapy in thoracic cancer patients; however, the exact molecular mechanisms remain unknown, and there is no effective treatment method in clinic. Here, we assessed the role of follistatin-like 1 (Fstl1) in RIPF.

A Multimodal Imaging Approach Based on Micro-CT and Fluorescence Molecular Tomography for Longitudinal Assessment of Bleomycin-Induced Lung Fibrosis in Mice.

Idiopathic pulmonary fibrosis (IPF) is a fatal lung disease characterized by the progressive and irreversible destruction of lung architecture, which causes significant deterioration in lung function and subsequent death from respiratory failure. The pathogenesis of IPF in experimental animal models has been induced by bleomycin administration. In this study, we investigate an IPF-like mouse model induced by a double intratracheal bleomycin instillation. Standard histological assessments used for studying l...

Sphingosine-1-phosphate receptor-2 facilitates pulmonary fibrosis through potentiating IL-13 pathway in macrophages.

Idiopathic pulmonary fibrosis is a devastating disease with poor prognosis. The pathogenic role of the lysophospholipid mediator sphingosine-1-phosphate and its receptor S1PR2 in lung fibrosis is unknown. We show here that genetic deletion of S1pr2 strikingly attenuated lung fibrosis induced by repeated injections of bleomycin in mice. We observed by using S1pr2LacZ/+ mice that S1PR2 was expressed in alveolar macrophages, vascular endothelial cells and alveolar epithelial cells in the lung and that S1PR2-ex...

The KCa3.1 blocker TRAM-34 inhibits proliferation of fibroblasts in paraquat-induced pulmonary fibrosis.

KCa3.1, a Ca-activated K channel, plays an important role in modulating calcium signaling and maintaining membrane potential during cell activation. It has been reported to promote fibroblast function in many fibrotic diseases. However, the role of KCa3.1 in the pathophysiology of pulmonary fibrosis after paraquat (PQ) poisoning has not been studied. A rat model of PQ poisoning was used. After treatment with TRAM-34, which is a highly selective KCa3.1 blocker, the expression of KCa3.1, TGF-β1 and α-SMA we...

Novel formononetin-7-sal ester ameliorates pulmonary fibrosis via MEF2c signaling pathway.

Pulmonary fibrosis is a progressive disorder with poor prognosis and limited treatment options. Therefore, novel therapeutic drugs should be developed in preclinical studies. In this study, we designed and synthesized a novel compound named formononetin-7-sal ester (FS). We also investigated its anti-pulmonary fibrosis ability on transforming growth factor beta 1 (TGF-β1)-stimulated pulmonary epithelial cells and fibroblasts in vitro and on bleomycin (BLM)-induced pulmonary fibrosis in vivo. FS strongly bl...

Therapeutic effect and mechanism of carboxyamidotriazole on the pulmonary fibrosis of mice induced by bleomycin.

To investigate the treatment effect of carboxyamidotriazole (CAI) on bleomycin induced lung fibrosis in mice, and the potential mechanism involved.A total of 45 mice were divided into three groups randomly. Blank control group (blank group): after a one-time tail vein injection of saline solution 0.2 ml, mice were given polyethylene glycol 400 (PEG-400) 0.1 ml/10 g by gavage once daily for 14 days; the bleomycin group (BLM group): after a one-time tail vein injection of bleomycin 150 mg/kg, mice were given ...


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