Silencing of long noncoding RNA H19 alleviates pulmonary injury, inflammation, and fibrosis of acute respiratory distress syndrome through regulating the microRNA-423-5p/FOXA1 axis

2021 ◽  
Vol 47 (4) ◽  
pp. 183-197
Author(s):  
Xianyu Mu ◽  
Hongrong Wang ◽  
Haiyong Li
Keyword(s):  
Acute Respiratory Distress Syndrome ◽  
Respiratory Distress Syndrome ◽  
Respiratory Distress ◽  
Long Noncoding Rna ◽  
Noncoding Rna ◽  
Distress Syndrome ◽  
Pulmonary Injury

scholarly journals Silencing of long noncoding RNA H19 alleviates pulmonary injury, inflammation and fibrosis in acute respiratory distress syndrome rats through regulating MicroRNA-423-5p

2020 ◽  
Author(s):  
Xianyu Mu ◽  
Hongrong Wang ◽  
Haiyong Li
Keyword(s):  
Acute Respiratory Distress Syndrome ◽  
Respiratory Distress Syndrome ◽  
Respiratory Distress ◽  
Long Noncoding Rna ◽  
Noncoding Rna ◽  
Distress Syndrome ◽  
Luciferase Reporter ◽  
Pulmonary Injury ◽  
Tnf Α ◽  
Histology Score

Abstract Background: This study aimed to explore the function of long noncoding RNA H19 (H19) on pulmonary injury, inflammation and fibrosis in lipoproteins (LPS)-induced acute respiratory distress syndrome (ARDS) rats. Methods: The LPS-induced ARDS rat model was established by intratracheal instillation with 2 mg/kg LPS. QRT-PCR was performed to detect the expression of H19, miR-423-5p, tumor necrosis factor-α (TNF-α), interleukin (IL)-1β, IL-6,, monocyte chemoattractant protein (MCP)-1 and vascular endothelial growth factor (VEGF). Histology score was detected by hematoxylin-eosin (HE) staining. Enzyme-linked immunosorbent assay (ELISA) was used to detect the levels of proinflammatory cytokines and the concentration of VEGF in bronchoalveolar lavage fluid (BALF). The protein expression of fiber factors was measured by western blot. The degree of fibrosis was observed by masson-trichrome staining. Dual-luciferase reporter assay was used to determine the binding site between miR-423-5p and H19.Results: The expression of H19 was significantly increased, while miR-423-5p was decreased in LPS-induced ARDS rats. Silencing of H19 decreased the mRNA expression of TNF-α, IL-1β, IL-6, MCP-1 and VEGF in LPS-induced ARDS rats, and decreased the levels of TNF-α, IL-1β, IL-6and the concentration of VEGF in BALF, histology score of LPS-induced ARDS rats. H19 inhibition also decreased the fibrosis score and the proteins expression of fiber factors of LPS-induced ARDS rats. Furthermore, miR-423-5p eliminated the effect of H19 on LPS-induced MH-S cells.Conclusions: Silencing of H19 ameliorated the pulmonary injury, inflammation and fibrosis of LPS-induced ARDS through regulating miR-423-5p, which may be a promising therapeutic strategy to treat ARDS.

Long noncoding plasmacytoma variant translocation 1 facilitates the surveillance of acute respiratory distress syndrome and mortality prediction in sepsis

2021 ◽  
Vol 15 (6) ◽  
pp. 401-412
Author(s):  
Yijue Liu ◽  
Huan Peng ◽  
Feng Gui
Keyword(s):  
Acute Respiratory Distress Syndrome ◽  
Respiratory Distress Syndrome ◽  
Respiratory Distress ◽  
Disease Severity ◽  
Noncoding Rna ◽  
Distress Syndrome ◽  
Mortality Prediction ◽  
Prediction Of Mortality ◽  
Failure Assessment ◽  
Variant Translocation

Aim: We aimed to investigate the association of long noncoding RNA plasmacytoma variant translocation 1 (lncRNA PVT1) expression with acute respiratory distress syndrome (ARDS) risk and its prognostic value for 28-day mortality in sepsis patients. Materials & methods: LncRNA PVT1 expression from 109 sepsis patients and 100 health controls was detected. General sepsis severity was assessed using acute physiology and chronic health evaluation II score and sequential organ failure assessment score. Results: LncRNA PVT1 had an acceptable predictive value for higher ARDS risk, then was identified as an independent risk factor for sepsis ARDS; LncRNA PVT1 expression positively correlated with general disease severity in sepsis patients; LncRNA PVT1 was overexpressed in 28-day deaths compared with 28-day survivors in sepsis patients. Conclusion: LncRNA PVT1 may facilitate the surveillance of ARDS, general disease severity and the prediction of mortality in sepsis patients.

scholarly journals Pendekatan Diagnosis Terbaru Vaping Associated Pulmonary Injury (VAPI)

2020 ◽  
Vol 2 (1) ◽  
pp. 74-80
Author(s):  
Anisa Ramadhanti
Keyword(s):  
Acute Respiratory Distress Syndrome ◽  
Respiratory Distress Syndrome ◽  
Respiratory Distress ◽  
Giant Cell ◽  
Interstitial Pneumonitis ◽  
Distress Syndrome ◽  
Organizing Pneumonia ◽  
Pulmonary Injury ◽  
Lipoid Pneumonia

Rokok elektronik atau vape diklaim lebih aman dan lebih tidak berbahaya karena lebih sedikit mengandung bahan kimia toksik dibandingkan rokok konvensional. Walaupun demikian, masih banyak pihak yang mempertanyakan keamanan rokok elektronik. Liquid dalam rokok elektronik dan aerosol yang dihasilkan terbukti mengandung sejumlah komponen kimia yang kemungkinan memiliki efek yang berbahaya terhadap kesehatan, terutama paru yang dapat menyebabkan vaping-associated pulmonary injury (VAPI). Berdasarkan laporan kasus sebelumnya, VAPI terbagi menjadi beberapa spektrum penyakit, diantaranya adalah pneumonia eosinofilik akut, organizing pneumonia, lipoid pneumonia, kerusakan alveolus difus, dan acute respiratory distress syndrome (ARDS), perdarahan alveolar difus, pneumonitis hipersensitif, dan yang paling jarang yaitu giant-cell interstitial pneumonitis. Terdapat definisi kasus yang terbaru dalam menegakkan diagnosis VAPI, serta tatalaksana

scholarly journals MiR-124-3p helps to protect against acute respiratory distress syndrome by targeting p65

2020 ◽  
Vol 40 (5) ◽  
Author(s):  
Yufeng Liang ◽  
Junjie Xie ◽  
Di Che ◽  
Chunmin Zhang ◽  
Yongmin Lin ◽  
...  
Keyword(s):  
Acute Respiratory Distress Syndrome ◽  
Respiratory Distress Syndrome ◽  
Respiratory Distress ◽  
Cell Apoptosis ◽  
Distress Syndrome ◽  
Direct Interaction ◽  
Pulmonary Injury ◽  
Nr8383 Cells

Abstract Background: Acute respiratory distress syndrome (ARDS) is a severe form of acute lung injury that has a high mortality rate and leads to substantial healthcare costs. MicroRNA-124-3p (miR-124-3p) helps to suppress inflammation during a pulmonary injury. However, its mechanism of action is largely unknown, and its role in ARDS remains to be determined. Methods: Mice and NR8383 cells were exposed to lipopolysaccharides (LPS) to induce ARDS, and their miR-124-3p levels were determined. After a miRNA agomir was administrated to the mice, their pulmonary injuries were evaluated by H&E staining and assays for peripheral inflammatory cytokine levels. The direct interaction between miR-124-3p and p65 was predicted, and then confirmed by a luciferase activity assay. The role played by miRNA-124-3p in regulating p65 expression was further examined by transfection with its agomir, and its role in cell apoptosis was investigated by observing the effects of miRNA overexpression in vitro and in vivo. Results: After exposure to LPS, there was a consistent decrease in miR-124-3p expression in the lungs of mice and in NR8383 cells. After treatment with the miR-124-3p agomir, the degrees of pulmonary injury (e.g. alveolar hemorrhage and interstitial edema), and the increases in IL-1β, IL-6, and TNF-α levels induced by LPS were significantly attenuated. Overexpression of miR-124-3p in NC8383 cells and lung tissues significantly suppressed LPS-induced p65 expression and cell apoptosis. Conclusions: These results suggest that miR-124-3p directly targeted p65, and thereby decreased the levels of inflammation and pulmonary injury in a mouse model of ARDS.

scholarly journals Acute respiratory distress syndrome caused by Mycoplasma pneumoniae in a child: the role of methylprednisolone and clarythromycin

2011 ◽  
Vol 9 (3) ◽  
pp. 386-388
Author(s):  
João Fernando Lourenço de Almeida ◽  
Adalberto Stape ◽  
Eduardo Juan Troster
Keyword(s):  
Acute Respiratory Distress Syndrome ◽  
Respiratory Distress Syndrome ◽  
Respiratory Distress ◽  
Mycoplasma Pneumoniae ◽  
Distress Syndrome ◽  
Pediatric Population ◽  
Pulmonary Injury ◽  
Good Recovery ◽  
Appropriate Use

ABSTRACT Mycoplasma pneumoniae is recognized as an important agent of pneumonia in pediatric population. In rare situations, severe pulmonary injury can develop. The use of corticoids in these cases remains controversial. A case of a girl with acute respiratory distress syndrome and bilateral pleural effusion secondary to pneumonia due to Mycoplasma pneumoniae is described, with good recovery after appropriate use of methylprednisolone and clarythromicyn.

Effect of Propofol and Dexmedetomidine on Pulmonary Injury in Patients with Acute Respiratory Distress Syndrome during Mechanical Ventilation

2021 ◽  
Vol 7 (4) ◽  
pp. 612-619
Author(s):  
Wei Liu ◽  
Wei Xu
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Mechanical Ventilation ◽  
Acute Respiratory Distress Syndrome ◽  
Respiratory Distress Syndrome ◽  
Respiratory Distress ◽  
Adverse Reactions ◽  
Distress Syndrome ◽  
Pulmonary Injury ◽  
Joint Group

Objective: This research intended to explore the role of propofol and dexmedetomidine on pulmonary injury in patients with acute respiratory distress syndrome (ARDS) during mechanical ventilation. Methods: A total of 150 ARDS patients undergoing mechanical ventilation in our hospital from January 2017 to May 2019 were randomly grouped into dexmedetomidine group (n=50), propofol group (n=50) and joint group (n=50). The changes of heart rate, systolic blood pressure, diastolic blood pressure in the three groups were compared. Elisa was applied to test the changes of inflammatory factors interleukin-6 (IL-6) and tumor necrosis factor-a (TNF-a) on the first, second and third days after mechanical ventilation. The pulmonary injury score before sedation and after sedation for 2 days (Table 2) was tested. Secondary outcome measures: the incidence of adverse reactions after anesthesia was observed. Results: After sedation, the mean artery pressure and heart rate of the three groups were significantly lower than those before sedation (P < 0.05). After sedation, the expressions of IL-6 and TNF-a in joint group were significantly lower than those in propofol and dexmedetomidine group (P < 0.05). Two-day pulmonary injury scores of the three groups showed that different sedation schemes had positive effects on improving pulmonary injury scores (P < 0.05), and the expressions of IL-6 and TNF-a declined with the decline of pulmonary injury scores. The incidence of adverse reactions in joint group was significantly higher than that in propofol group and dexmedetomidine group (P < 0.05). Conclusion: Propofol and dexmedetomidine can effectively improve the effect of pulmonary injury in ARDS patients during mechanical ventilation, and slow down the occurrence of inflammatory reaction, which is an effective scheme of sedation in clinical mechanical ventilation.

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