Parthenolide attenuated bleomycin-induced pulmonary fibrosis via the NF-κB/Snail signaling pathway

Li, Xiaohe; Tu, Xiao; Yang, Jiahuan; Qin, Yuan; Gao, Jingjing; Liu, Huijuan

doi:10.1186/s12931-018-0806-z

Cited by 50 publications

(26 citation statements)

References 34 publications

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“…MIGLITOL CTD 00002031, CHEMBL55802 CTD 00003118, hesperidin CTD 00006087, cytochalasin D CTD 00007076, prolinedithiocarbamate CTD 00002658, parthenolide CTD 00000087, FEXOFENADINE HYDROCHLORIDE CTD 00003191, hydroxytyrosol CTD 00000267, antimycin A CTD 00005427, anacardic acid C15:3 CTD 00003117 are the peak drug candidates for COVID-19 and IPF. Parthenolide demonstrates role of anti-inflammatory activities against IPF [ 54 ] that proves the efficiency of the proposed drugs. The current study uses a number of Bioinformatics methodologies in GSE147507, which indicates SARS-CoV-2 infection in human lung epithelium cell and GSE35145 compare sample between affected and normal IPF tissue of humans.…”

Section: Discussionmentioning

confidence: 97%

Network-based identification genetic effect of SARS-CoV-2 infections to Idiopathic pulmonary fibrosis (IPF) patients

Taz

Ahmed

Paul

et al. 2020

Briefings in Bioinformatics

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Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is accountable for the cause of coronavirus disease (COVID-19) that causes a major threat to humanity. As the spread of the virus is probably getting out of control on every day, the epidemic is now crossing the most dreadful phase. Idiopathic pulmonary fibrosis (IPF) is a risk factor for COVID-19 as patients with long-term lung injuries are more likely to suffer in the severity of the infection. Transcriptomic analyses of SARS-CoV-2 infection and IPF patients in lung epithelium cell datasets were selected to identify the synergistic effect of SARS-CoV-2 to IPF patients. Common genes were identified to find shared pathways and drug targets for IPF patients with COVID-19 infections. Using several enterprising Bioinformatics tools, protein–protein interactions (PPIs) network was designed. Hub genes and essential modules were detected based on the PPIs network. TF-genes and miRNA interaction with common differentially expressed genes and the activity of TFs are also identified. Functional analysis was performed using gene ontology terms and Kyoto Encyclopedia of Genes and Genomes pathway and found some shared associations that may cause the increased mortality of IPF patients for the SARS-CoV-2 infections. Drug molecules for the IPF were also suggested for the SARS-CoV-2 infections.

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Section: Discussionmentioning

confidence: 97%

Network-based identification genetic effect of SARS-CoV-2 infections to Idiopathic pulmonary fibrosis (IPF) patients

Taz

Ahmed

Paul

et al. 2020

Briefings in Bioinformatics

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“…These effects of PTL in tumors and inflammatory diseases primarily happen via the inhibition of NF-κB signaling pathways (Hehner et al, 1999). Current studies have established that PTL inhibit pulmonary fibrosis increasing E-Cadherin and decreasing vimentin NF-κB and Snail expression in TGF-β1-treated primary lung epithelial cells (Li et al, 2018a).…”

Section: Introductionmentioning

confidence: 99%

Natural Plants Compounds as Modulators of Epithelial-to-Mesenchymal Transition

et al. 2019

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Epithelial-to-mesenchymal transition (EMT) is a self-regulated physiological process required for tissue repair that, in non-controled conditions may lead to fibrosis, angiogenesis, loss of normal organ function or cancer. Although several molecular pathways involved in EMT regulation have been described, this process does not have any specific treatment. This article introduces a systematic review of effective natural plant compounds and their extract that modulates the pathological EMT or its deleterious effects, through acting on different cellular signal transduction pathways both in vivo and in vitro . Thereby, cryptotanshinone, resveratrol, oxymatrine, ligustrazine, osthole, codonolactone, betanin, tannic acid, gentiopicroside, curcumin, genistein, paeoniflorin, gambogic acid and Cinnamomum cassia extracts inhibit EMT acting on transforming growth factor-β (TGF-β)/Smads signaling pathways. Gedunin, carnosol, celastrol, black rice anthocyanins, Duchesnea indica , cordycepin and Celastrus orbiculatus extract downregulate vimectin, fibronectin and N-cadherin. Sulforaphane, luteolin, celastrol, curcumin, arctigenin inhibit β-catenin signaling pathways. Salvianolic acid-A and plumbagin block oxidative stress, while honokiol, gallic acid, piperlongumine, brusatol and paeoniflorin inhibit EMT transcription factors such as SNAIL, TWIST and ZEB. Plectranthoic acid, resveratrol, genistein, baicalin, polyphyllin I, cairicoside E, luteolin, berberine, nimbolide, curcumin, withaferin-A, jatrophone, ginsenoside-Rb1, honokiol, parthenolide, phoyunnanin-E, epicatechin-3-gallate, gigantol, eupatolide, baicalin and baicalein and nitidine chloride inhibit EMT acting on other signaling pathways (SIRT1, p38 MAPK, NFAT1, SMAD, IL-6, STAT3, AQP5, notch 1, PI3K/Akt, Wnt/β-catenin, NF-κB, FAK/AKT, Hh). Despite the huge amount of preclinical data regarding EMT modulation by the natural compounds of plant, clinical translation is poor. Additionally, this review highlights some relevant examples of clinical trials using natural plant compounds to modulate EMT and its deleterious effects. Overall, this opens up new therapeutic alternatives in cancer, inflammatory and fibrosing diseases through the control of EMT process.

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“…The epithelial-to-mesenchymal transition of pulmonary fibrosis is induced through the TGF- β /smad signaling pathway [ 14 ]. Parthenolide is able to influence the level of EMT-related proteins and to treat pulmonary fibrosis by affecting the progression of pulmonary fibrosis through the NF- κ B/Snail signaling pathway [ 15 ]. Therefore, EMT, NF- κ B, and related inflammatory factors (TGF- β , TNF- α , and IL) are very important in the evaluation of pulmonary fibrosis.…”

Section: Introductionmentioning

confidence: 99%

Imrecoxib Inhibits Paraquat-Induced Pulmonary Fibrosis through the NF-κB/Snail Signaling Pathway

Huang¹

2020

Computational and Mathematical Methods in Medicine

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Objective. In recent years, pulmonary fibrosis caused by paraquat poisoning is still concerned. However, no effective drugs have been developed yet to treat paraquat-induced pulmonary fibrosis. The aim of our research is to investigate whether imrecoxib can inhibit paraquat-induced pulmonary fibrosis and its possible mechanism. Methods. Extraction of primary pulmonary fibrosis cells (PPF cells) in vitro by the method of trypsin digestion. RT-qPCR and western blot were employed to measure the transcription level and protein expression of EMT related markers in paraquat-induced A549 cells. MTT, wound-healing, and Transwell experiments were used to verify the effect of imrecoxib on the proliferation, migration, and invasion of PPF and HFL1 cells. Results. Firstly, our results confirmed that paraquat can induce EMT and activate the NF-κB/snail signal pathway in lung epithelial cell A549. Furthermore, experimental results showed that imrecoxib could repress the proliferation, migration, and invasion of PPF and HFL1 cells. Finally, our study found that imrecoxib can inhibit EMT of paraquat-induced A549 cells by the NF-κB/snail signal pathway. Conclusion. Imrecoxib can inhibit EMT of paraquat-induced A549 cells and alleviate paraquat-caused pulmonary fibrosis through the NF-κB/snail signal pathway. Therefore, imrecoxib is a drug worthy of study in the treatment of paraquat-induced pulmonary fibrosis.

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Parthenolide attenuated bleomycin-induced pulmonary fibrosis via the NF-κB/Snail signaling pathway

Cited by 50 publications

References 34 publications

Network-based identification genetic effect of SARS-CoV-2 infections to Idiopathic pulmonary fibrosis (IPF) patients

Network-based identification genetic effect of SARS-CoV-2 infections to Idiopathic pulmonary fibrosis (IPF) patients

Natural Plants Compounds as Modulators of Epithelial-to-Mesenchymal Transition

Imrecoxib Inhibits Paraquat-Induced Pulmonary Fibrosis through the NF-κB/Snail Signaling Pathway

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