Experimental Models of Pulmonary Fibrosis and their Translational Potential

Abstract

Pulmonary fibrosis, represented mainly by idiopathic pulmonary fibrosis, develops chronic and progressive changes in lung parenchyma with high mortality and limited therapeutic options. The aim of this review was to summarize the most common experimental models used in the research of pulmonary fibrosis. Lung damage associated with development of pulmonary fibrosis can be caused by irradiation or by instillation of bleomycin, fluorescein isothiocyanate (FITC), silicon dioxide (silica), asbestos, etc. This article reviews the characteristics of the most frequently used animal models of fibrosis, including the limitations of their use. Although none of the used animal models resembles completely the changes in human pulmonary fibrosis, similarities between them allow preclinical testing of novel treatment approaches or their combinations in the laboratory conditions before their use in the clinical practice.

Effect of Cov-Pla1 and Cov-Pla3 extract on some pulmonary function parameters in rabbits

“…This results in acute alveolitis and interstitial inflammation actively characterized by recruitment of neutrophils, lymphocytes, and macrophages in the acute phase (Hoshino et al, 2009). This acute inflammatory injury may occur in a timeframe as short as 24 hours followed by reversible fibrosis (Matute-Bello et al, 2008;Moeller et al, 2008;Jana et al, 2019) and closely resembles acute lung injury (ALI) (Mouratis et al, 2011).…”

The mitigating effect of para‐hydroxycinnamic acid in bleomycin‐induced pulmonary fibrosis in mice through targeting oxidative, inflammatory and fibrotic pathways

“…Free electrons combine with oxygen to create superoxide or hydroxyl radicals, which attack DNA phosphodiester links, breaking strands and causing chromosomal abnormalities. 54 Hence, to assess the potential antioxidant properties of the test agents (PFD and P-HCA), the levels of oxidative markers (MDA, GSH, SOD and GPx) associated with lung injury were quantified. The findings of this investigation demonstrated a significant decrease in the oxidative MDA level in lung tissue and an increase in the antioxidant GSH and GPx in animals treated with P-HCA compared to those in the group induced with BLM.…”

“…According to published reports, bleomycin directly damages cells by oxidizing iron to bleomycin–Fe 3+ . Free electrons combine with oxygen to create superoxide or hydroxyl radicals, which attack DNA phosphodiester links, breaking strands and causing chromosomal abnormalities 54 . Hence, to assess the potential antioxidant properties of the test agents (PFD and P‐HCA), the levels of oxidative markers (MDA, GSH, SOD and GPx) associated with lung injury were quantified.…”

До Патогенезу Експериментального Фіброзу Легень У Тварин (Клініко- Гематологічні Дослідження)

“…Впродовж останнього часу було розроблено різні моделі фіброзу легень. Серед них більш використовувані: променеве ураження легень; інсталяція блеоміцину, кремнію або азбесту; метод використання трансгенних мишей або перенесення генів із застосування фіброгенних цитокінів [2,3].…”