Perfluorocarbon attenuates inflammatory cytokines, oxidative stress and histopathologic changes in paraquat-induced acute lung injury in rats

Khalighi, Zahra; Rahmani, Asghar; Cheraghi, Javad; Ahmadi, Mohammad Reza; Soleimannejad, Koroush; Ruhangiz, Asadollahi; Asadollahi, Khairollah

doi:10.1016/j.etap.2015.12.002

Cited by 24 publications

(16 citation statements)

References 28 publications

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“…Moreover, studies have shown that paraquat can activate inflammatory related factors including TNF α , NF- κ B, interleukin 1 β , and IL-6, which in turn contribute to the development of pulmonary fibrosis [ 26 ]. NF- κ B is a crucial transcription regulator, which plays an extremely important function in the process of inflammation, immunity, and apoptosis.…”

Section: Discussionmentioning

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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Section: Discussionmentioning

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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“…Since the first PQ poisoning death in the 1960s, PQ poisoning has begun to increase (14). It has many infection routes, with strong toxicity and rapid poisoning time (15). This is also an important reason for clinical attention.…”

Section: Discussionmentioning

confidence: 99%

Effects of paraquat on IL‑6 and TNF‑α in macrophages

2018

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Effects of paraquat (PQ) on interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α) in macrophages were investigated. Different concentrations of PQ were added to mouse macrophage RAW264.7 for culture. According to different concentrations of PQ, mice were divided into micro concentration (0.01 mmol/l), low concentration (0.1 mmol/l), medium concentration (1 mmol/l), high concentration (10 mmol/l), and control groups without PQ. Trypan blue solution was used for detecting cell viability, a microplate reader for detecting the fluorescence intensity of reactive oxygen species (ROS), ELISA for detecting the expression levels of IL-6 and TNF-α. The medium concentration and the high concentration groups had significantly lower cell viability than the other three groups (P<0.050). The high concentration group had significantly lower cell viability than the medium concentration group (P<0.050). At 1, 4 and 8 h, respectively, the medium and the high concentration groups had significantly higher ROS fluorescence intensity than the other three groups (P<0.050). The high concentration group had significantly higher ROS fluorescence intensity than the medium concentration group (P<0.050). There were significant differences in the expression levels of IL-6 and TNF-α at the 1st, 4th and 8th hour among the five groups (P<0.050). In the micro, the low, the medium and high concentration groups, the expression levels of IL-6 and TNF-α were the lowest at 1 h and the highest at 8 h, which were higher at 4 h than those at 1 h (P<0.050). PQ at a concentration of 1 mmol/l can produce toxicity to macrophages, and greatly increase the ROS fluorescence intensity, the expression levels of IL-6 and TNF-α. PQ poisoning is expected to be treated though IL-6 and TNF-α in the future.

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“…Although the toxicity of paraquat for fish is low, exposure to high doses or prolonged contact with low concentrations of paraquat may also cause a severe toxicity to vital organs, primarily the liver, gills and kidney [1][2][3][4]. Toxicological properties of paraquat are attributed to its ability to produce reactive oxygen species such as superoxide anion that may directly or indirectly cause cell death [2,5]. Damage to cells or cell death may lead to changes in blood biochemical parameters [6].…”

Section: Introductionmentioning

confidence: 99%

Effects of Sub-Lethal Toxicity of Paraquat on Blood Biochemical Parameters of Common Carp, Cyprinus carpio (Linnaeus, 1758)

Banaee

Behzad

Somayeh

et al. 2016

IJT

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Perfluorocarbon attenuates inflammatory cytokines, oxidative stress and histopathologic changes in paraquat-induced acute lung injury in rats

Cited by 24 publications

References 28 publications

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

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

Effects of paraquat on IL‑6 and TNF‑α in macrophages

Effects of Sub-Lethal Toxicity of Paraquat on Blood Biochemical Parameters of Common Carp, Cyprinus carpio (Linnaeus, 1758)

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