Objective: To observe the expression of 5-Hydroxytryptamine 2B receptor (5-HTR2B)、E-cadherin (E-cad)、alpha-smooth muscle actin(α-SMA) in the bleomycin -induced pulmonary fibrosis tissue of rats.
Methods: Forty-five healthy male SD rats were randomly di-vided into control group,bleomycin group and bleomycin+prednisone group(=15). Five rats in each group randomly sacrificed at the 7、the 14 and the 28 day after eastablishing models. The lung tissue was observed by microscope in HE and Masson staining. Lung hydroxypro-line (HYP) content was evaluated. The expression of protein and mRNA of 5-HTR2B, E-cad and α-SMA were analyzed by immunohistoche-mistry and/or RT-PCR.
Results: A dynamic changes from alveolitis to pulmonary fibrosis could be observed in the slices by HE and Masson staining. The experimental results by immunohistochemistry and RT-PCR showed that the protein and mRNA expression of 5-HTR2B and a-SMA enhanced rat pulmonary fibrosis (<0.05) and reached the highest at the 28 day; the corresponding protein and mRNA expression of E-cad reduced (<0.05), and reduced to the lowest value at the 28 day. Compared with bleomycin group, the corresponding mRNA and protein expression of 5-HTR2B and a-SMA in bleomycin+prednisone group had decreased (<0.05); however, the corresponding mRNA and protein expression of E-cad had increased(<0.05).
Conclusions: 5-HTR2B is involved in the pathogenesis of pulmonary fibrosis throught epithelial-mesenchymal transition (EMT).
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http://dx.doi.org/10.13459/j.cnki.cjap.2016.04.020 | DOI Listing |
Microb Cell Fact
January 2025
Pharmaceutical Microbiology Department, Faculty of Pharmacy, Tanta University, Tanta, 31527, Egypt.
Carbapenem-resistant Klebsiella pneumoniae poses a severe risk to global public health, necessitating the immediate development of novel therapeutic strategies. The current study aimed to investigate the effectiveness of the green algae Arthrospira maxima (commercially known as Spirulina) both in vitro and in vivo against carbapenem-resistant K. pneumoniae.
View Article and Find Full Text PDFJ Cyst Fibros
January 2025
Cystic Fibrosis Therapeutics Development Network Coordinating Center, Seattle Children's Hospital, Seattle, WA, USA; Department of Pediatrics, University of Washington, Seattle, WA, USA; Department of Biostatistics, University of Washington, Seattle, WA, USA.
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View Article and Find Full Text PDFRespir Med
January 2025
Division of Pulmonology, Department of Internal Medicine, Myongji Hospital, Hanyang University College of Medicine, Gyeonggi-do, Republic of Korea. Electronic address:
Introduction: Ca2+ signaling in fibroblasts would be one of the important mediators of lung fibrosis. This study investigated the relationship between calcium channel blocker usage and the risk of developing interstitial lung disease and idiopathic pulmonary fibrosis.
Material And Methods: This cohort study used data from the Korean National Health Screening Cohort spanned from January 1, 2004, to December 31, 2015.
Life Sci
January 2025
Department of Biological Sciences (Regulatory Toxicology), National Institute of Pharmaceutical Education and Research (NIPER), Balanagar, Hyderabad, TS 500037, India. Electronic address:
Pulmonary fibrosis (PF) arises from dysregulated wound healing, leading to excessive extracellular matrix (ECM) deposition and impaired lung function. Macrophages exhibit high plasticity, polarizing to pro-inflammatory M1 during early inflammation and anti-inflammatory, fibrosis-inducing M2 during later stages of PF. Additionally, neutrophils and neutrophil extracellular traps (NETs) release mediated by peptidyl arginine deiminase (PAD-4), also play a key role in PF progression.
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January 2025
Department of Histology and Embryology, Erciyes University, Faculty of Medicine, 38039 Kayseri, Turkey. Electronic address:
Favipiravir, a broad-spectrum RNA-dependent RNA polymerase inhibitor widely used during the COVID-19 pandemic, effectively reduces viral load but has been linked to inflammatory changes in tissues such as the liver and kidneys. High-dose and prolonged use of favipiravir for COVID-19 raises concerns about its potential toxic effects on the lungs, particularly in patients with pre-existing pulmonary conditions. This study investigated favipiravir's effects on lung tissue in healthy rats.
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