Pyrrolidinedithiocarbamate attenuates bleomycin-induced pulmonary fibrosis in rats: Modulation of oxidative stress, fibrosis, and inflammatory parameters

Zaafan, Mai A.; Zaki, Hala F.; El-Brairy, Amany I.; Kenawy, Sanaa A.

doi:10.1080/01902148.2016.1244578

Cited by 20 publications

(16 citation statements)

References 12 publications

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“…In our study, elevated hydroxyproline content in CBs‐treated lung tissues suggested that CBs could induce collagen synthesis. In agreement with our study, studies also suggested that there was a positive relation between hydroxyproline level and pathological grade of bleomycin‐induced pulmonary fibrosis 22 …”

Section: Discussionsupporting

confidence: 93%

ROCK inhibitor attenuates carbon blacks‐induced pulmonary fibrosis in mice via Rho/ROCK/NF‐kappa B pathway

Yan

Tang

Zhong

et al. 2021

Environmental Toxicology

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Exposure to carbon blacks (CBs) has been associated with the progression of pulmonary fibrosis, whereas the mechanism is still not clear. We therefore aimed to investigate the effect of RhoA/ROCK pathway on pulmonary fibrosis caused by CBs exposure. Western blot analysis indicated that CBs could promote the activation of RhoA/ROCK pathway and phosphorylation of p65 and IκBα in mice lung. However, ROCK inhibitor Y‐27632 could attenuate phosphorylation levels of p65 and IκBα and restore histopathological changes of the lung tissue. Then, we evaluated the effect of RhoA/ROCK pathway on pulmonary fibrosis by detecting the expression levels of α‐SMA, vimentin, and Collagen type‐I (Col‐I), which could be partly inhibited by Y‐27632. It was assumed that inhibition of ROCK could be a promising therapeutic candidate for CBs‐induced pulmonary fibrosis, which possibly through the blockage of RhoA/ROCK/NF‐κB pathway.

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Section: Discussionsupporting

confidence: 93%

ROCK inhibitor attenuates carbon blacks‐induced pulmonary fibrosis in mice via Rho/ROCK/NF‐kappa B pathway

Yan

Tang

Zhong

et al. 2021

Environmental Toxicology

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“…The hyperplasia of fibroblasts was increasingly evident with time and has been associated with chronic inflammatory reaction (21,22). Recent research has indicated that TNF-α and TGF-β1 promotes the development of inflammation and pulmonary fibrosis (66,67).…”

Section: Discussionmentioning

confidence: 99%

The influence of PM2.5 on lung injury and cytokines in mice

Yang

Chen

et al. 2019

Exp Ther Med

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Exposure to particulate matter ≤2.5 µm in diameter (PM2.5) profoundly affects human health. However, the role of PM2.5 on lung injury and cytokine levels in mice is currently unknown. The aim was to examine the effect of PM2.5 pollution on lung injury in mice fed at an underground parking lot. A total of 20 female Kunming mice were randomly divided into control and polluted groups, with 10 rats in each group. The control group was kept in the laboratory, while the pollution group was fed in an underground parking lot. The concentrations of pollutants were measured using ambient air quality monitoring instruments. After 3 months of treatment, the lungs were collected and examined using electron microscopy, and the morphological structures were assessed using hematoxylin and eosin staining. The polarization of macrophages was evaluated by immunofluorescence. The concentration of interleukin (IL)-4, tumor necrosis factor (TNF)-α and transforming growth factor (TGF)-β1 in peripheral sera were assessed by ELISA. The mRNA and protein levels of IL-4, TNF-α, and TGF-β1 in lung tissues were assessed by reverse transcription-quantitative polymerase chain reaction and western blot analyses, respectively. In the polluted group, the levels of CO, NOx and PM2.5 were significantly higher compared with the control group. Compared with the controls, intracellular edema, an increased number of microvilli and lamellar bodies, smaller lamellar bodies in type II alveolar epithelial cells, and abundant particles induced by PM2.5 in macrophages were observed in the polluted group. The lung ultrastructure changed in the polluted group, revealing exhaust-induced lung injury: The tissues were damaged, and the number of inflammatory cells, neutrophils, polylymphocytes and eosinophils increased in the polluted group compared with the control group. The authors also observed that the number of M1 and M2 macrophages markedly increased after the exhaust treatment. The levels of IL-4, TNF-α and TGF-β1 in the sera and tissues were significantly increased in the polluted group. PM2.5 pollutants in underground garages can lead to lung injury and have a significant impact on the level of inflammatory cytokines in mice. Therefore, the authors suggest that PM2.5 can activate the inflammatory reaction and induce immune dysfunction, leading to ultrastructural damage.

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“…Bleomycin-induced pulmonary fibrosis in mice is a highly reproducible in vivo model to induce consistent pulmonary fibrosis. The bleomycin induces the production of free radicals by binding to iron and DNA and causes DNA, lipid, and protein damage, leading to the activation of inflammatory and fibrotic responses in the lung (20). Thus, we established a bleomycin-induced fibrosis model to evaluate the anti-fibrotic effect of morin.…”

Section: Discussionmentioning

confidence: 99%

Protective Effects of Morin Against Bleomycin-Induced Pulmonary Fibrosis in Mice

Hemmati

Pashmforosh

Tabandeh

et al. 2019

Jundishapur J Nat Pharm Prod

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Background: Idiopathic pulmonary fibrosis (IPF) is a fatal and incurable lung disease. Morin, a natural product with antioxidant and anti-inflammatory activity, could reduce lung inflammation induced by lipopolysaccharide (LPS) and liver fibrosis in previous studies. Objectives: The aim of this study was to evaluate the antifibrotic activity of morin in the pulmonary fibrosis induced by bleomycin in mice. Methods: Pulmonary fibrosis was induced by the intratracheal instillation of bleomycin (3 mg/kg) in C57Bl/6J mice. Morin (10, 20, and 40 mg/kg, p.o.) was given to mice from day 0 to 21 after bleomycin administration. The mice were sacrificed on day 21 to measure the total number of cells, the percentage of leukocytes in bronchoalveolar lavage fluid (BALF), lung hydroxyproline content, lung index, and oxidative stress markers. Histopathological changes were evaluated by the microscopic examination of sections stained with hematoxylin-eosin and Masson's trichrome. Results: Our data showed that treatment with morin significantly attenuated the infiltration of inflammatory cells, hydroxyproline content, lung index, and oxidative stress that were elevated in fibrotic lungs. In addition, morin could reduce the pathological changes induced by bleomycin. Conclusions: Based on the study, morin, probably by its anti-inflammatory and antioxidant activities, can attenuate pulmonary fibrosis induced by bleomycin in mice.

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Pyrrolidinedithiocarbamate attenuates bleomycin-induced pulmonary fibrosis in rats: Modulation of oxidative stress, fibrosis, and inflammatory parameters

Abstract: PDTC attenuated bleomycin-induced pulmonary fibrosis in rats via its anti-inflammatory, antioxidant, and antifibrotic activities.

Cited by 20 publications

References 12 publications

ROCK inhibitor attenuates carbon blacks‐induced pulmonary fibrosis in mice via Rho/ROCK/NF‐kappa B pathway

ROCK inhibitor attenuates carbon blacks‐induced pulmonary fibrosis in mice via Rho/ROCK/NF‐kappa B pathway

The influence of PM2.5 on lung injury and cytokines in mice

Protective Effects of Morin Against Bleomycin-Induced Pulmonary Fibrosis in Mice

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